Category Archives: Stem Cell Medical Center


F.D.A. Approves 2 Sickle Cell Treatments, One Using CRISPR Gene Editing – The New York Times

On Friday, the Food and Drug Administration approved the first gene editing therapy ever to be used in humans, for sickle cell disease, a debilitating blood disorder caused by a single mutated gene.

The agency also approved a second treatment using conventional gene therapy for sickle cell that does not use gene editing.

For the 100,000 Americans with the disease, most of them Black, the approvals offer hope for finally living without an affliction that causes excruciating pain, organ damage and strokes.

While patients, their families and their doctors welcome the F.D.A.s approvals, getting either therapy will be difficult, and expensive.

It is practically a miracle that this is even possible, said Dr. Stephan Grupp, chief of the cellular therapy and transplant section at Childrens Hospital of Philadelphia. Dr. Grupp, who consults for Vertex, said his medical center was hoping to begin treating sickle cell patients next year.

But, he added, I am very realistic about how hard this is.

The obstacles to treatment are myriad: an extremely limited number of medical centers authorized to provide it; the requirement that each patients cells be edited or have a gene added individually; procedures that are so onerous that not everyone can tolerate them; and a multimillion-dollar price tag and potential insurance obstacles.

As a result, sickle cell experts said, only a small fraction of patients in the United States are expected to receive the new treatment (to say nothing of the millions of sickle cell patients overseas, particularly in Africa, for whom it may be completely out of reach for now). The F.DA. estimates that about 20,000 patients who are 12 and older and have had episodes of debilitating pain will be eligible for the therapies.

The gene editing treatment, called Exa-cel and using the brand name Casgevy, was jointly developed by Vertex Pharmaceuticals of Boston and CRISPR Therapeutics of Switzerland. It uses CRISPR, the Nobel Prize-winning gene editing tool, to snip patients DNA. For a small number of subjects in clinical trials, it corrected the effects of the mutation, which results in red blood cells that are shaped like sickles or crescents that become caught in blood vessels, blocking them.

Casgevy is the first treatment to be approved that uses CRISPR. Patients will also need expensive, intensive medical care and a long hospitalization.

The other treatment, called Lyfgenia and made by Bluebird Bio of Somerville, Mass., uses a common gene therapy method to add a good hemoglobin gene to patients DNA.

Vertex says its price to edit a patients genes will be $2.2 million; for, Bluebird it will be $3.1 million.

But living with the disease is also extremely costly: On average, $1.7 million for those with commercial insurance over a patients lifetime. Patients themselves may pay about $44,000 out of pocket on average over the course of their lives.

For patients and the doctors who treat them, it is tantalizing to think of being free from the complications of sickle cell. So despite the many unknowns, medical centers say they are compiling lists of interested patients who are ready to pursue treatment when it becomes available.

We are talking for the first time about survivorship, said Dr. Sharl Azar, medical director of the comprehensive sickle cell disease treatment center at Massachusetts General Hospital. Patients, said Dr. Azar, who previously consulted for Vertex, are starting to hope they can live into their 70s and 80s rather than dying young.

Treatment will start with hospital visits to collect patients bone marrow stem cells the precursors of red blood cells that are treated to enable the production of healthy blood cells. Stem cells must be released from the marrow into the blood so they can be collected. To release them, doctors inject patients with a drug, plerixafor.

It can take months to get enough stem cells to send to a central facility for treatment. And Vertex has only one gene editing facility in the United States, in Tennessee, and one in Europe, in Scotland. Bluebirds facility is in New Jersey.

After editing a patients cells with CRISPR, technicians do a sequence of quality checks. About 16 weeks after the process begins, the cells will be shipped back to the medical center to be infused into the patient, said Dr. Julie Kanter, director of the adult sickle cell center at the University of Alabama at Birmingham.

At that point, doctors must clear the patients marrow with intensive chemotherapy to make way for the new cells. Patients remain in the hospital for a month or more while their edited stem cells repopulate their marrows, during which time they have no functioning immune system.

That is if they can find a medical center that offers the new therapy. Most hospitals will not be able to offer Casgevy even if they want to. So far, Vertex has authorized only nine centers to provide its treatment. The company says it will eventually authorize about 50.

Bluebird has 27 authorized centers and also plans to add more.

The gene editing treatment is so challenging and requires so many resources that leading medical centers say that even if they are authorized to provide it they would probably only be able to treat a small number of patients a year.

We cant do more than 10 a year, said Dr. Kanter, who has in the past consulted for Vertex and Bluebird Bio.

And, Dr. Kanter said, were really good at it, adding that her medical center had extensive experience treating sickle cell patients and participating in the Bluebird clinical trials.

Others said the same. Five to 10 a year, said Dr. Jean-Antoine Ribeil, clinical director of the Center of Excellence in Sickle Cell Disease at Boston Medical Center, which says it is the largest sickle cell center in New England and is one approved by Vertex to offer its therapy.

Vertex has not revealed how many patients cells it will be able to edit each year, saying only that it is confident it can meet the demand at the time the treatment is introduced.

Nor has Bluebird. But, Dr. Grupp said, Bluebirds gene therapy for thalassemia a genetic disorder in which the body does not make enough hemoglobin gives a hint. Bluebird, he said, has only been able to treat the cells of 50 patients a year since the drug was approved in August 2022. And that is for the entire country, Dr. Grupp said.

Insurance payments pose another obstacle. Before treatment starts, a patients insurer has to agree to pay. That can take months, said Dr. David Jacobsohn, chief of the division of blood and marrow transplantation at Childrens National Hospital in Washington. His medical center is among those authorized to provide the Vertex and the Bluebird treatments.

Most sickle cell patients are insured through Medicaid, noted Dr. John DiPersio, director of the Center for Gene and Cellular Immunotherapy at the Washington University School of Medicine in St. Louis. Dr. DiPersio consults for Vertex and Bluebird.

If every sickle cell patient in Missouri gets treated, the state couldnt afford it, he said.

Another concern involves unknowns about the new therapy. While a panel of F.D.A. experts concluded that the benefits outweighed the risks, doctors remain mindful of unexpected outcomes.

We dont know yet what the long-term effects will be, Dr. DiPersio said. We havent followed patients long enough just a couple of years. And stem cells, he added, will live forever, so if CRISPR or the Bluebird gene therapy does genetic damage, it will remain.

Haja Sandi, a 19-year-old student at Rowan University in New Jersey, hopes to be at the top of the list at the Childrens Hospital of Philadelphia.

She has frequent hospitalizations for pain so intense she has to take morphine. Her symptoms have forced her into remote schooling. There is no way I could do it in person, she said.

Hearing about the Vertex therapy, she contacted the hospital in Philadelphia asking if she could get it.

God willing, I will go forward with it, she said.

The Childrens Hospital of Philadelphia, among others, is hoping to get on Vertexs list of approved centers and is planning to take eligible patients on a first-come-first-served basis.

Still others, like Childrens National Hospital in Washington, will give priority to the sickest patients.

Dr. Azar intends to take a different approach if Massachusetts General is approved. He said he wanted to proceed with extreme caution, starting with just one patient and going through the entire process before accepting more.

He worries that a misstep could sully the treatment for those who could be helped.

Going forward, the therapies will be provided without the extensive support that the companies gave to clinical trial participants. And it will be a test case for using CRISPR gene editing to treat other diseases. CRISPR Therapeutics is now studying gene editing to treat cancer, diabetes, and A.L.S., among others.

It is a blessing and curse that we are going first, Dr. Azar said. Sickle cell disease has never been first for anything.

The people seeking the therapy mostly Black patients often mistrust the health care system, he added.

We want to do this right, Dr. Azar said. We dont want patients to feel like they are guinea pigs.

Continued here:
F.D.A. Approves 2 Sickle Cell Treatments, One Using CRISPR Gene Editing - The New York Times

Impact of disease burden on clinical outcomes of AML patients … – Nature.com

Dhner H, Estey E, Grimwade D, Amadori S, Appelbaum FR, Bchner T, et al. Diagnosis and management of AML in adults: 2017 ELN recommendations from an international expert panel. Blood. 2017;129:42447. https://doi.org/10.1182/blood-2016-08-733196.

Article CAS PubMed PubMed Central Google Scholar

Heuser M, Freeman SD, Ossenkoppele GJ, Buccisano F, Hourigan CS, Ngai LL, et al. 2021 Update on MRD in acute myeloid leukemia: a consensus document from the European LeukemiaNet MRD Working Party. Blood. 2021;138:275367. https://doi.org/10.1182/blood.2021013626.

Article CAS PubMed PubMed Central Google Scholar

Schuurhuis GJ, Heuser M, Freeman S, Bene MC, Buccisano F, Cloos J, et al. Minimal/measurable residual disease in AML: a consensus document from the European LeukemiaNet MRD Working Party. Blood. 2018;131:127591. https://doi.org/10.1182/blood-2017-09-801498.

Article CAS PubMed PubMed Central Google Scholar

Nagler A, Baron F, Labopin M, Polge E, Esteve J, Bazarbachi A, et al. Measurable residual disease (MRD) testing for acute leukemia in EBMT transplant centers: a survey on behalf of the ALWP of the EBMT. Bone Marrow Transpl. 2021;56:21824. https://doi.org/10.1038/s41409-020-01005-y.

Article Google Scholar

Buckley SA, Wood BL, Othus M, Hourigan CS, Ustun C, Linden MA, et al. Minimal residual disease prior to allogeneic hematopoietic cell transplantation in acute myeloid leukemia: a meta-analysis. Haematologica. 2017;102:86573. https://doi.org/10.3324/haematol.2016.159343.

Article CAS PubMed PubMed Central Google Scholar

Walter RB, Gooley TA, Wood BL, Milano F, Fang M, Sorror ML, et al. Impact of pretransplantation minimal residual disease, as detected by multiparametric flow cytometry, on outcome of myeloablative hematopoietic cell transplantation for acute myeloid leukemia. J Clin Oncol. 2011;29:11907. https://doi.org/10.1200/jco.2010.31.8121.

Article PubMed PubMed Central Google Scholar

Araki D, Wood BL, Othus M, Radich JP, Halpern AB, Zhou Y, et al. Allogeneic hematopoietic cell transplantation for acute myeloid leukemia: time to move toward a minimal residual disease-based definition of complete remission? J Clin Oncol. 2016;34:32936. https://doi.org/10.1200/jco.2015.63.3826.

Article PubMed Google Scholar

Zhou Y, Othus M, Araki D, Wood BL, Radich JP, Halpern AB, et al. Pre- and post-transplant quantification of measurable (minimal) residual disease via multiparameter flow cytometry in adult acute myeloid. Leuk Leuk. 2016;30:145664. https://doi.org/10.1038/leu.2016.46.

Article CAS Google Scholar

Ustun C, Courville EL, DeFor T, Dolan M, Randall N, Yohe S, et al. Myeloablative, but not reduced-intensity, conditioning overcomes the negative effect of flow-cytometric evidence of leukemia in acute myeloid leukemia. Biol Blood Marrow Transplant: J Am Soc Blood Marrow Transplant. 2016;22:66975. https://doi.org/10.1016/j.bbmt.2015.10.024.

Article Google Scholar

Morsink LM, Bezerra ED, Othus M, Wood BL, Fang M, Sandmaier BM, et al. Comparative analysis of total body irradiation (TBI)-based and non-TBI-based myeloablative conditioning for acute myeloid leukemia in remission with or without measurable residual disease. Leukemia. 2020;34:17015. https://doi.org/10.1038/s41375-019-0671-x.

Article PubMed Google Scholar

Morsink LM, Sandmaier BM, Othus M, Palmieri R, Granot N, Bezerra ED, et al. Conditioning intensity, pre-transplant flow cytometric measurable residual disease, and outcome in adults with acute myeloid leukemia undergoing allogeneic hematopoietic cell transplantation. Cancers. 2020;12:2339.

Article CAS PubMed PubMed Central Google Scholar

Gilleece MH, Labopin M, Yakoub-Agha I, Volin L, Soci G, Ljungman P, et al. Measurable residual disease, conditioning regimen intensity, and age predict outcome of allogeneic hematopoietic cell transplantation for acute myeloid leukemia in first remission: A registry analysis of 2292 patients by the Acute Leukemia Working Party. Eur Soc Blood Marrow Transplant Am J Hematol. 2018;93:114252. https://doi.org/10.1002/ajh.25211.

Article Google Scholar

Schlenk RF, Dhner K, Mack S, Stoppel M, Kirly F, Gtze K, et al. Prospective evaluation of allogeneic hematopoietic stem-cell transplantation from matched related and matched unrelated donors in younger adults with high-risk acute myeloid leukemia: German-Austrian trial AMLHD98A. J Clin Oncol. 2010;28:46428. https://doi.org/10.1200/jco.2010.28.6856.

Article PubMed Google Scholar

Duval M, Klein JP, He W, Cahn JY, Cairo M, Camitta BM, et al. Hematopoietic stem-cell transplantation for acute leukemia in relapse or primary induction failure. J Clin Oncol. 2010;28:37308. https://doi.org/10.1200/jco.2010.28.8852.

Article PubMed PubMed Central Google Scholar

Le Bourgeois A, Labopin M, Marais A, de Latour RP, Blaise D, Chantepie S, et al. Sequential allogeneic hematopoietic stem cell transplantation for active refractory/relapsed myeloid malignancies: results of a reduced-intensity conditioning preceded by clofarabine and cytosine arabinoside, a retrospective study on behalf of the SFGM-TC. Ann Hematol. 2020;99:185562. https://doi.org/10.1007/s00277-020-04074-7.

Article CAS PubMed Google Scholar

Malard F, Labopin M, Stuhler G, Bittenbring J, Ganser A, Tischer J, et al. Sequential intensified conditioning regimen allogeneic hematopoietic stem cell transplantation in adult patients with intermediate- or high-risk acute myeloid leukemia in complete remission: a study from the Acute Leukemia Working Party of the European Group for Blood and Marrow Transplantation. Biol Blood Marrow Transplant: J Am Soc Blood Marrow Transplant. 2017;23:27884. https://doi.org/10.1016/j.bbmt.2016.11.002.

Article Google Scholar

Schmid C, Schleuning M, Ledderose G, Tischer J, Kolb HJ. Sequential regimen of chemotherapy, reduced-intensity conditioning for allogeneic stem-cell transplantation, and prophylactic donor lymphocyte transfusion in high-risk acute myeloid leukemia and myelodysplastic syndrome. J Clin Oncol. 2005;23:567587. https://doi.org/10.1200/jco.2005.07.061.

Article PubMed Google Scholar

Pfrepper C, Klink A, Behre G, Schenk T, Franke GN, Jentzsch M, et al. Risk factors for outcome in refractory acute myeloid leukemia patients treated with a combination of fludarabine, cytarabine, and amsacrine followed by a reduced-intensity conditioning and allogeneic stem cell transplantation. J Cancer Res Clin Oncol. 2016;142:31724. https://doi.org/10.1007/s00432-015-2050-y.

Article CAS PubMed Google Scholar

Kebriaei P, Kline J, Stock W, Kasza K, Le Beau MM, Larson RA, et al. Impact of disease burden at time of allogeneic stem cell transplantation in adults with acute myeloid leukemia and myelodysplastic syndromes. Bone Marrow Transpl. 2005;35:96570. https://doi.org/10.1038/sj.bmt.1704938.

Article CAS Google Scholar

Thol F, Gabdoulline R, Liebich A, Klement P, Schiller J, Kandziora C, et al. Measurable residual disease monitoring by NGS before allogeneic hematopoietic cell transplantation in AML. Blood. 2018;132:170313. https://doi.org/10.1182/blood-2018-02-829911. e-pub ahead of print 2018/09/08.

Article CAS PubMed Google Scholar

Jentzsch M, Grimm J, Bill M, Brauer D, Backhaus D, Schulz J, et al. Prognostic relevance of remission and measurable residual disease status in AML patients prior to reduced intensity or non-myeloablative allogeneic stem cell transplantation. Blood Cancer J. 2021;11:80 https://doi.org/10.1038/s41408-021-00471-x.

Article PubMed PubMed Central Google Scholar

Lachowiez CA, Atluri H, DiNardo CD. Advancing the standard: venetoclax combined with intensive induction and consolidation therapy for acute myeloid leukemia. Ther Adv Hematol. 2022;13:20406207221093964 https://doi.org/10.1177/20406207221093964.

Article PubMed PubMed Central Google Scholar

Stelljes M, Middeke JM, Bug G, Wagner E-M, Mueller LP, Christoph S, et al. In patients with relapsed/refractory AML sequential conditioning and immediate allogeneic stem cell transplantation (allo-HCT) results in similar overall and leukemia-free survival compared to intensive remission induction chemotherapy followed by Allo-HCT: results from the randomized phase III ASAP trial. Blood. 2022;140:911. https://doi.org/10.1182/blood-2022-159962.

Article Google Scholar

Bazarbachi A, Bug G, Baron F, Brissot E, Ciceri F, Dalle IA, et al. Clinical practice recommendation on hematopoietic stem cell transplantation for acute myeloid leukemia patients with FLT3-internal tandem duplication: a position statement from the Acute Leukemia Working Party of the European Society for Blood and Marrow Transplantation. Haematologica. 2020;105:150716. https://doi.org/10.3324/haematol.2019.243410.

Article CAS PubMed PubMed Central Google Scholar

Bazarbachi A, Labopin M, Battipaglia G, Djabali A, Passweg J, Soci G, et al. Sorafenib improves survival of FLT3-mutated acute myeloid leukemia in relapse after allogeneic stem cell transplantation: a report of the EBMT Acute Leukemia Working Party. Haematologica. 2019;104:e398e401. https://doi.org/10.3324/haematol.2018.211615.

Article CAS PubMed PubMed Central Google Scholar

Abou Dalle I, El Cheikh J, Bazarbachi A. Pharmacologic strategies for post-transplant maintenance in acute myeloid leukemia: it is time to consider! Cancers. 2022; 14. https://doi.org/10.3390/cancers14061490.

Read this article:
Impact of disease burden on clinical outcomes of AML patients ... - Nature.com

CancerVAX CEO Ryan Davies Discusses Cancer Research with Leading Pediatric Hematologic Oncologist – Yahoo Finance

Dr. Satiro De Oliveira, a principal investigator in the Companys cancer research program at UCLA, comments about the importance of cancer immunotherapy

LEHI, Utah, April 12, 2023 (GLOBE NEWSWIRE) -- CancerVAX, Inc., developer of a breakthrough universal cancer vaccine that will use the bodys immune system to fight cancer, reported that CEO Ryan Davies spoke about the importance of cancer immunotherapy with Dr. Satiro De Oliveira, a principal investigator in the Companys cancer research program at UCLA.

Dr. De Oliveira is a board-certified pediatrician and board-certified pediatric hematology/oncologist. He received his medical degree in Brazil and completed his pediatric residency at Woodhull Medical and Mental Health Center in New York and his pediatric hematology/oncology fellowship at the Childrens Hospital Lost Angeles. His clinical focus is on pediatric oncology and gene therapies and his research focus is on cancer immunotherapy and biology of stem cell transplantation.

In addition to his impressive educational background, Dr. De Oliveira has received numerous awards, including the Certificate of Congressional Recognition, the STOP CANCER Research Career Development Award, and the American Society of Hematology Scholar Award. Outside of clinical practice, Dr. De Oliveira conducts clinical research on gene therapies in the fields of adoptive immunotherapy, pediatric hematopoietic stem cell transplantation, and pediatric red blood cell hematology, to name a few.

As a pediatric oncology specialist, Dr. De Oliveiras work impacts patients lives in real time. During the conversation, Dr. De Oliveira emphasized the impact of recent clinical research strides on his patients, As I meet the families, I say, Listen, 10 years ago, this disease wouldve killed this child. And now, this patient is a miracle, Were really building the history of medicine.

CancerVax CEO Ryan Davies commented, It was a pleasure speaking with Dr. De Oliveira. His thought about creating the history of medicine is a beautiful thing.

Story continues

This Podcast can be viewed athttps://youtu.be/DcFor_Vo4MU

For more information about CancerVax, please visithttp://www.cancervax.com/.

About Us

CancerVAX, Inc. is a pre-clinical biotechnology company developing a breakthrough universal cancer vaccine that will use the bodys immune system to fight cancer. Working with a team of experienced cancer researchers and physicians at UCLA, we intend to create a Universal Cancer Vaccine that will detect, mark, and destroy only the diseased cells with an incredibly high level of precision. Much like the COVID-19 vaccines that train the body to recognize and destroy the coronavirus, our cancer vaccine will leverage the bodys own immune system to destroy cancer cells. As we develop our universal cancer vaccine, we are also working with UCLA to develop single-disease cancer treatments targeting Ewing sarcoma, a rare but deadly bone and soft tissue cancer that primarily affects children and young adults. We look forward to the day when treating cancer will be as simple as getting a flu shot.

Forward-Looking Statements

This press release may contain forward-looking statements within the meaning of the safe harbor provisions of the U.S. Private Securities Litigation Reform Act of 1995. Forward-looking statements are neither historical facts nor assurances of future performance. Instead, they are based only on our current beliefs, expectations and assumptions regarding the future of our business, future plans and strategies, projections, anticipated events and trends, the economy and other future conditions. Because forward-looking statements relate to the future, they are subject to inherent uncertainties, risks and changes in circumstances that are difficult to predict and many of which are outside of our control. Our actual results and financial condition may differ materially from those indicated in the forward-looking statements. Therefore, you should not rely on any of these forward-looking statements. Any forward-looking statement made by us in this release is based only on information currently available to us and speaks only as of the date on which it is made. We undertake no obligation to publicly update any forward-looking statement, whether written or oral, that may be made from time to time, whether as a result of new information, future developments or otherwise.df

Press Contact:CancerVAX, Inc.Tel: (805) 356-1810communications@CancerVAX.com

See the original post:
CancerVAX CEO Ryan Davies Discusses Cancer Research with Leading Pediatric Hematologic Oncologist - Yahoo Finance

EW GROUP SHINES AT 12TH A4M SYMPOSIUM 2023 & "ALL-ON … – PR Newswire

BANGKOK, April 11, 2023 /PRNewswire/ -- European Wellness Biomedical Group (EW Group) made a successful showing at an exclusive event, the 12th A4M Symposium 2023, which was held in Centara, Bangkok, 16th-19th February 2023.

The two-day A4M Symposium, commenced with a welcome ceremony featuring Dr. Manus Potaporn (Deputy Director General of Medical Services Department, Thailand) as a Guest of Honour, hosted by Prof. Dr. Mike Chan (A4M Thailand President), Dr. Jakkriss Bumisawasdi (A4M Thailand Honorary President), and Dr. Robert Goldman (A4M Founder).

On February 19, European Wellness Academie (EWA), a non-profitable educational arm of EW Group, brought an exclusive workshop, "All-On Bioregen Optimization," to explore the world of anti-aging and regenerative medicine, featured some of the world's leading anti-aging experts.

Prof. Dr. Mike Chan, presented his two topics, "The Application of Regenerative Precursor Stem Cells, Peptides & Exosomes in Precision Medicine" and "Phyto-Myco-based Nano Organo Peptides: A New Trend in Precision Medicine."

"Precision Medicine in Age Reversal," which brought together the anti-aging and wellness industries on a single platform to achieve Precision Medicine's goals, which are patient-centred, may divide patients into subgroups based on their illness vulnerability, prognosis, or response to a specific treatment. It is devised and administered after comprehensive diagnostics utilizing Panomic Analysis and System Biology to analyse the patient's state at a molecular level and apply targeted therapies to address illness progression.

Anti-aging medicine aims to improve human ageing and maximize physical and mental well-being. Scientific data and medical journals supported the model's focus on Advanced Clinical Preventive and Regenerative Medicine.

The involvement of the healthcare and wellness industries will have a significant influence on the anti-aging sector for many years to come. Yet, by fact these sectors worked together to improve the quality of life for individuals and will contribute to defining the very future of modern medicine.

European Wellness Biomedical Group

An award-winning European group, most renowned for its pioneering development in organ-specific precursor (progenitor) stem cell therapeutics, biological and synthetic peptides, biological regenerative medicine, immunotherapies, and nutraceutical and cosmeceuticals.

EW Group's multinational business divisions include research and developments, bio-manufacturing, biomedical academies, hospital and wellness centres and nutraceutical product distribution across 80 countries worldwide. EW Group also owns and operates a growing network of internationally accredited Hospital and Medical Centres specializing in Regenerative Bio-Medicine and luxury Wellness Centres globally. EW Group is headquartered in Germany and Malaysia (Asia Pacific) with research vested in Germany, Switzerland, Czech Republic and United Kingdom.

Home

Media Contact:Ferellica Anne Martin+6088 448 989 (Ext: 337)[emailprotected]

SOURCE European Wellness Biomedical Group

Follow this link:
EW GROUP SHINES AT 12TH A4M SYMPOSIUM 2023 & "ALL-ON ... - PR Newswire

care team inspires hope for cancer patient | UT Health East Texas – UT Health East Texas

Jim Jordan returned from a golfing trip in August knowing something wasnt quite right with his health. After undergoing bloodwork, which had been perfect at a visit in March, he was told he needed to go to the emergency room immediately. He and his wife, Becky, arrived at UT Health Tyler, not knowing what exactly was wrong or what to expect.

Dr. Lance Mandell, who specializes in oncology and hematology at UT Health East Texas HOPE Cancer Center, soon told them that Jim, 64, had myelodysplastic syndrome (MDS), which can transition to acute myeloid leukemia.

We didnt know anybody, thank God he was on call. We were blessed to get Dr. Mandell, Becky said. From the time he sat down with us that first night, we were scared. He talked to us 20 or 30 minutes, sitting on the end of the bed. Hes been the best.

Despite their shock, the Jordans said Dr. Mandell provided them comfort and hope that first night.

From Day 1 he said, Weve got this, Jim said of that first meeting with Dr. Mandell. He said, Not only are we going to get this, were going to cure this.

Jim started outpatient chemotherapy at HOPE Cancer Center, but his MDS did turn into leukemia and he eventually was admitted to UT Health Tyler to help him fight off infection while he underwent additional treatments.

That feeling of hope and comfort the Jordans felt the first night of Jims diagnosis continued with hospital staff for the six weeks he spent in the hospital.

This is the best group of nurses weve ever been around, and weve been around, Becky said. Every single one of them. Ive never seen anything like it, its totally remarkable.

Becky stayed with Jim almost every night he was in the hospital, heading to their Henderson home only to do laundry and check on their two Shih Tzus.

The nurses just took such good care of him. I didnt worry a minute. And thats not me, I worry all the time about him, she said. I have never seen anything like this group here. They are on the ball, and they explain and tell us in detail what theyre doing and why with a smile on their face. They are so on the ball here, they are heaven.

Alex McComas, RN, said the entire nursing staff formed a bond with Jim, playfully fighting over who got to care for him each day.

There were days when he was really sick, and you could tell he didnt feel good but wanted to have a good attitude, she said. It makes you appreciative of all the things you can do to take care of him and to encourage him to keep going.

In turn, Alex said, Jim often encouraged those who were caring for him.

Hes been so encouraging to us despite the position hes in. He doesnt have to encourage the nursing, staff but he does, she said. Thats been the biggest gift to see and be a part of. Its been the biggest honor to take care of him and learn from him.

Dr. Mandell said that attitude can make a difference. Hes been the perfect patient. Attitude makes a huge, huge difference and hes had the most positive attitude I think Ive ever seen, he said.

Because of that attitude and the bond he developed with all of his caregivers, the staff decided to present Jim with a blanket crocheted by the mother-in-law of David Warren, a cancer survivor who works at UT Health East Texas in the facilities department.

She wanted someone that really was deserving of it, someone that was going through a hard time, Warren said.

His mother-in-law, Connie French, said she made the blanket as a remembrance to her husband, who she lost to cancer in 2007.

Cancer took my husband. Ive got to fight it somehow, so Im doing what I can, French said. Its from the heart. Ive got to do something. I cant do it any other way, so thats what I do, I crochet.

Jim teared up as he accepted the blanket, presented by his team of caregivers the day he was discharged.

Its been scary and something you never want to go through, but theyve just been so good, he said. Theres not one thing I would change. Every day they were my motivation. They saved my life.

Now in remission, Jim will face a stem cell transplant at UT Health Southwestern in hopes of keeping the cancer from ever returning. He plans to keep in touch with his UT Health East Texas care team, who became such a part of his life, and throw them a party when he returns.

All the people here have been nothing but good, they helped me every day through it, Jim said. The whole floor has been unbelievable and helpful, they got us through it.

Originally posted here:
care team inspires hope for cancer patient | UT Health East Texas - UT Health East Texas

Available Therapies for US Patients With R/R B-Cell Lymphoma – Targeted Oncology

Tycel Phillips, MD, associate professor, Division of Lymphoma, Department of Hematology & Hematopoietic Cell Transplantation, discusses treatment options for diffuse large B-cell lymphoma in the Unites States [US].

0:08 | At the current moment, if we look at patients with relapsed refractory diffuse large B cell lymphoma, which is the most common non-Hodgkin lymphoma in the US in that setting, we had several approved agents in the last several years. So, there was an oral medication lenalidomide [Revlimid] given together with an antibody called tafasitamab, and that is approved for patients [in] second-line or beyond, especially those in second-line who are unable to tolerate more traditional treatments. In that second-line space, we have historically had salvage chemotherapy, and the complications that we know come with that, followed by autologous stem cell transplantation. For a large number of patients, salvage chemo and autologous transplant was not a great option because these patients had intrinsic resistance to chemotherapy.

1:00 | More recently, we had the approval of 2 chimeric antigen receptor therapy treatments, or CAR T treatment. CAR T, as much as we advocate for it, is also available in the third-line is underutilized here in the US with only about a third of patients who are eligible for CAR T, or making it to CAR T. So, there's a large number of patients who cannot get to this treatment either because they do not live near a CAR T center or they don't want to travel to a CAR T center, or they can't keep their disease under control enough to get to CAR T.

1:29 | As of right now, CAR T is probably the only treatment that has durable responses in this patient population. So, with those other treatments that I didn't mention, there's probably a minority of those patients who will have a durable response. But the vast majority of those patients will likely relapse and die from the cancer, and if they can't get the CAR Tt that does leave a large number of patients who are at need, which prompts the need for more treatments in his patient population. Because even with CAR T, as much as I have advocated for have in this you know earlier in this conversation, about half of those patients, if not a little bit more, will fail to respond to CAR T or relapse after treatment with CAR T, and those patients have very poor outcomes as well.

The rest is here:
Available Therapies for US Patients With R/R B-Cell Lymphoma - Targeted Oncology

Roundtable Discussion: Ziari Assesses Therapy Sequencing in … – Targeted Oncology

Mohammadbagher Ziari, MD

Assistant Clinical Professor

Department of Medical Oncology & Therapeutics Research

City of Hope

Corona, CA

CASE SUMMARY

A 70-year-old woman received a diagnosis of stage I multiple myeloma. She had a medical history of stage 3 chronic kidney disease and moderate renal impairment, and fluorescence in situ hybridization testing showed deletion 17p. The patient declined autologous stem cell transplantation and received lenalidomide (Revlimid), bortezomib (Velcade), and dexamethasone (RVd). Her best response was a very good partial response (VGPR), and lenalidomide maintenance continued.

Two years later she had her first relapse while on lenalidomide maintenance. On routine follow-up, the patient reported having mild fatigue, but continued to work full time. Her bone marrow plasma cells, light chains, and M protein were rising while her kidney function was worsening, and she now has stage IV chronic kidney disease. The patient received daratumumab (Darzalex) plus pomalidomide (Pomalyst) with a best response of VGPR. One year later a second relapse was discovered, and her kidney function continued to decline.

DISCUSSION QUESTIONS

ZIARI: Based on the NCCN [National Comprehensive Cancer Network] guidelines, there are preferred regimens for [patients with] early relapses with 1 to 3 prior treatments. If the patient has a relapse after more than 6 months, the regimen used primarily can be repeated. Patients who are still sensitive to bortezomib and lenalidomide have options that include ixazomib [Ninlaro], lenalidomide, and dexamethasone, which is a category 1 recommendation, and then RVd.

For bortezomib-refractory patients, one can use any of the regimens that have lenalidomide or a combination of daratumumab, carfilzomib [Kyprolis], and dexamethasone. For patients with lenalidomide-refractory disease, you can do daratumumab, carfilzomib, and dexamethasone; or daratumumab, bortezomib, and dexamethasone; or isatuximab [Sarclisa], carfilzomib, and dexamethasone.1

CHALLAGALLA: Most of them are exposed in my practice already. So in this patient, if shes still not going to go to stem cell transplant or CAR [chimeric antigen receptor] T-cell therapy, I think I would go with isatuximab, carfilzomib, and dexamethasone.

SOLANKI: Theres still selinexor [Xpovio] and other drugs. This has become such a chronic disease.

ZIARI: RightI mean, now that your patient has relapsed with Dara-Pd. We have used the anti-CD38, the IMiD, and the PI. The unmet need seems to be a new agent, probably with a different mechanism of action.

BHANDARI: I think this is when we start getting into either sending the patient for some trials at a tertiary center or sending the patient maybe for evaluation for CAR T-cell therapy or another BCMA [B-cell maturation antigen] type of therapy.

DISCUSSION QUESTION

ZIARI: What do you consider? Is there any other MOA that you think we need to address?

ARJUNAN: Yes, I think thats always a thought in my mind when were switching therapies. In this patient, I think you certainly would be looking at switching MOA, so you kind of think about selinexor, elotuzumab [Empliciti], and some of those other drugs out there. The big concern I have, regardless of the MOA, is the tolerance issue. It becomes worrisome trying to get these patients who are a little bit beat up on their first line of therapies onto some of these other ones.

ZIARI: You touched a great point, exactly. We have other regimens that are recommended like bortezomib, liposomal doxorubicin, and dexamethasone or carfilzomib and dexamethasone. There is CyBorD [cyclophosphamide (Cytoxan), bortezomib, dexamethasone]; carfilzomib, cyclophosphamide, and dexamethasone; or ixazomib, cyclophosphamide, and dexamethasone. Also, [we have] selinexor, bortezomib, and dexamethasone, or other selinexor-based regimens such as daratumumab and dexamethasone.

We also have venetoclax (Venclexta) and dexamethasone only in [patients with] t(11;14). Elotuzumab, pomalidomide, and dexamethasone is another option for a patient who had an IMiD [immunomodulatory drug] and PI [proteasome inhibitor] and progressed within 60 days of completion of last treatment. Pomalidomide and dexamethasone is category 1, and selinexor, pomalidomide, and dexamethasone is another option. There are other older regimens like DCEP [dexamethasone, cyclophosphamide, etoposide (Toposar), cisplatin (Platinol)].1 I dont know if any of you have used it recently, but I know that a long time ago I used it, but not anymore.

DISCUSSION QUESTIONS

ZIARI: You have used RVd and the patient was on maintenance lenalidomide and then progressed in 2021 [after 2 years]. After the first relapse, the patient was on Dara-Pd and now that you have utilized those MOAs that we talked about, it comes to the second relapse. Now you have options like an XPO1 inhibitor and CAR T-cell therapy, an anti-BCMA, or others. We have used a PI, anti-CD38, and IMiD.

MAZHARUDDIN: Well one thought that comes to mind is that the patient seems to have been off the bortezomib when they progressed. So it kind of opens the potential of reintroducing a proteasome inhibitor.

CHALLAGALLA: I agree with that. I think I would use carfilzomib, selinexor, and dexamethasone.

ZIARI: Would you do selinexor, bortezomib, and dexamethasone?

CHALLAGALLA: [This patient] doesnt have any history of cardiomyopathy or CHF [congestive heart failure]. Id like to avoid neuropathy. I would still try to push her toward stem cell transplant or CAR T-cell therapy because she does not seem to be refractory but is just relapsing.

SOLANKI: In the BOSTON trial [NCT03110562], most of the patients had been exposed to multiple agents. But they reintroduced bortezomib in those patients, and some of them got it within the last 6 to 9 months or less than 1 year, and they still showed a response. In fact, in the [bortezomib and dexamethasone] arm of the study, there was a response to bortezomib.2 So if [this patient] is otherwise suitableI dont know what her creatinine clearance is, was it good enough for CAR T-cell therapy?

ZIARI: Yes, youre correct.

DISCUSSION QUESTION

ZIARI: There is the genetic risk, like deletion 17p. Also, patient comorbidities like renal impairment and hypertension, or prior toxicities such as neuropathy. Is neuropathy something that you see in your patient after you use triple regimen for 2 lines of therapy? Is it something that you see despite using subcutaneous proteasome inhibitors? Is this something that is a challenge in your practice?

KANNAN: Its concerning. I think it affects their quality of life because its a chronic disease. Most of my patients develop it with bortezomib-based therapy at first-line therapy, so it tends to be a major problem.

ZIARI: What do you think, Dr Kannan, about the regimen that you would choose for your patient who had 2 lines of triple treatment in the past and now youre going to third-line therapy? What would you use?

KANNAN: Sometimes Ive done carfilzomib-based therapy because theyve had RVd followed by Dara-Pd. Ive tried selinexor. I push them toward CAR T-cell therapy, obviously if they are not refractory, but I still dont understand why this patient did not have a bone marrow transplant. Or did they have a transplant in between? If they have not had a transplant, they should be considered for transplant with the option of CAR T-cell therapy for the future, but I would collaborate with my [transplant physician] for them.

ZIARI: How far [away] is the transplant or CAR T-cell therapy center?

KANNAN: 20 miles.

ZIARI: I see; not bad, not bad at all. The MOA is important, too, if your patient has progressed on a treatment. If you use something new, think of the safety, exactly as you mentioned about neuropathy and different safety issues. We want to just use something that will not only keep the longevity but also the quality of life the same as much as we can. Always consider cost to the patient too: how much is out of their pocket and the distance theyre dealing with. I dont know how much geography is a problem when it comes to using oral regimen vs not oral regimen. Is it something concerning if the patient lives far away from you?

KANNAN: I dont think distance is a problem, but cost can be a major problem in our patient population, which is a little bit lower socioeconomically, and that affects [adherence].

ZIARI: That is true in every single practice, and you feel it more in the community practice.

CASE UPDATE

The patient was started on selinexor plus Vd based on her worsening renal impairment, deletion 17p status, and prior therapies. She achieved a VGPR.

DISCUSSION QUESTIONS

ARJUNAN: Ive used it once. We ran out of options for the patient. I was working in conjunction with [The University of Texas] MD Anderson [Cancer Center]. It was tough. A lot of fatigue, diarrhea as well, and it was quite a lot of monitoring.

ZIARI: Did you use it after multiple lines orin combination with bortezomib or anything else?

ARJUNAN: I used it after multiple lines.

ZIARI: You used it as a doublet treatment with dexamethasone or with bortezomib?

ARJUNAN: Yes, a doublet treatment with dexamethasone.

CHALLAGALLA: Ive used it as a doublet treatment, too, in an elderly person with terrible neuropathy. The indication was triplet therapy with bortezomib, but there was no way I could use bortezomib, so I did the 80-mg selinexor with dexamethasone.

I mean, its a different mechanism, except you must watch out for hyponatremia in this older population from the nausea, vomiting, and diarrhea, and I think we are all pretty good with the hematologic toxicities. We are pretty good at treating them. I think its the neurologic toxicity and the hyponatremia that we need to be careful of.

ZIARI: I have the same experience that you both had before. Just the hyponatremia is something to monitor closely, and fatigue too.

ZIARI: The BOSTON study data showed the efficacy and the adverse effects [AEs] of selinexor. Some of you have experience with it and some of you dont. But based on the data, how would you discuss this with your patient?

BHANDARI: Were there any patients on dialysis on that study?

ZIARI: They included patients who had kidney function less than 40%,2 so patients on dialysis [were] included.

ARJUNAN: Yes, so I think its a discussion about the data, to some extent. What concerns me about these data is that [the study] used, in my opinion, kind of a comparator arm that was questionable. About 70% of the patients had prior exposure to bortezomib already and then theyre using that as a comparator arm, so its kind of like youre expecting that comparator arm to fail, basically. I dont see what the data show me beyond telling the patient, Hey, maybe let us add selinexor, which has a different mechanism of action. It might help you. But I think when were looking at the data, its hard to use that as a convincing reason.

I dont know if there was, perhaps, a better comparator arm that could have been used in this trial instead of Vd alone. But otherwise, its about discussing the AEs and just counseling [the patients] through that. It is kind of difficult because with the other options you might have other toxicities. [As with] belantamab [Blenrep], you have the ophthalmic toxicity. So its weighing what the patient would be tolerant to.

ZIARI: I think there are data that we have also that compared pomalidomide, bortezomib, and dexamethasone with Vd. Also, they did a similar [study] but with Dara-Vd vs Vd and looked at the PFS [progression-free survival] difference too. I guess for the data that we have, the control arm was the old regimen that in the past had been a standard. Thats the reason that they always have something in addition to the doublet, with a different MOA to see if it is better than the standard.

DISCUSSION QUESTIONS

CHALLAGALLA: We always dose reduce. Nausea/vomiting is easily controlled, but we dose reduce if there [will] be AEs.

ZIARI: For the dose that we reduce to, there are data about that dose, so that you dont lose the efficacy. Have you used olanzapine [as an antiemetic]?

CHALLAGALLA: Thats the problem I have with all these drugs. There is no drop in efficacy by dose reduction, so why do we have to use the full dose and make the patient suffer?

ZIARI: In the BOSTON study, most patients had [dose modifications] eventually. You can always lower the dose too. This is what weve learnedthat maybe a lower dose is not a problem. I mean, again, in the BOSTON study, eventually they had most patients on the 80-mg dose.

SOLANKI: This question came up way back when panobinostat [Farydak] was introduced. It clearly disappeared mainly because it had severe GI [gastrointestinal] toxicity, mainly diarrhea. This has been a recurring problem with drugs, like now with selinexor. What Dr Challagalla pointed out is a recurring theme. We say, Oh well, 70% of the patients had to have dose reductions. Well, how did we come up with this dose in the first place?

The same thing happened with bortezomib way back. We used to use much higher doses, and then we went to weekly dosing. It turns out that the total dose of bortezomib we give is considerably less than what was originally used, and we still see wonderful responses. So theres a significant issue with the starting dose that is used in trials. Nobody seems to report what was the delivered dosehow much did the patient get, not what was planned.

ZIARI: In the BOSTON study they did. The majority [of patients received] 80 mg.

SOLANKI: I think what happened with the BOSTON [From the Data2] trial was because of the design, it became a once-a-week regimen of selinexor, and that considerably decreased the GI toxicity. Still, there was considerable dose reduction in those patients. So its still a pretty tough drug, although I was surprised how effective the combination was in patients who were penta refractory. Even in the Vd arm, there was a response rate of about 35% or 30% which is remarkable, so it was an interesting study, but not an easy one on the patients.

ZIARI: I have patients on this and I have been dose reducing, even down to 40 mg and they still have a response to it. I have 2 patients currently on it and down to 40 mg once a week, and I see the efficacy. I had to dose reduce to different things. But one other thing I do is olanzapine on day 1 of the treatment, and then I do it for 3 days in a row. I ask the patient how they feel after 3 days. If theyre fine, then I just ask them to use it as needed. If you do it days 1 to 3, and 1 hour before the starting day, then continue for 3 days or use a different cocktail plus hydration, it pretty much gets easier. Typically, after the first 2 months, the patient tolerates it and the AEs get less and less.3

DISCUSSION QUESTION

CHALLAGALLA: My choice would depend on the comorbidities of the patient. If the patient has severe neuropathy, bortezomib is out. Cardiomyopathy, carfilzomib is out, or kidney disease too. If theyve been exposed to daratumumab, I dont think I would use any anti-CD38 drug again because I dont believe that reusing it is going to be helpful. I dont know whats the right answer. It depends on the patient. In my practice, if I have used RVd and then daratumumab, etc, then XKd [selinexor, carfilzomib, and dexamethasone] seems most reasonable because if the same patient had kidney disease, I would have probably used pomalidomide before.

ZIARI: I see. So if you want to use a combination with selinexor, where do you think it fits in your line of treatment?

CHALLAGALLA: One can use selinexor and dexamethasone. One could use anything. We have so many choices right now, and we must weigh the AEs and patients comorbidities, then choose. Thats the way I would think.

ZIARI: Thats correct. We have great choices available now, but youre talking about a different MOA when you use selinexor. Weve pretty much run out of many other MOAs, and we were thinking about something new.

REFERENCES

NCCN. Clinical Practice Guideline in Oncology. Multiple Myeloma, version 1.2023. Accessed February 22, 2023. https://bit.ly/3KqmxUF

Grosicki S, Simonova M, Spicka I, et al. Once-per-week selinexor, bortezomib, and dexamethasone versus twice-per-week bortezomib and dexamethasone in patients with multiple myeloma (BOSTON): a randomised, open-label, phase 3 trial. Lancet. 2020;396(10262):1563-1573. doi:10.1016/S0140-6736(20)32292-3

Xpovio. Prescribing information. Karyopharm Therapeutics Inc; 2020. Accessed February 22, 2023. https://bit.ly/3eG0OqV

Continued here:
Roundtable Discussion: Ziari Assesses Therapy Sequencing in ... - Targeted Oncology

Immunology Center of Georgia recruits reflect expertise from … – Jagwire Augusta

Immune cells that can smell the metabolites of a high-fat Western diet and may produce inflammation and ultimately heart disease as a result, just what our longer RNAs are doing in our bodies and the role of immune cells called neutrophils in both cancer and heart disease are some areas of pursuit of the first five scientists recruited to the new Immunology Center of Georgia at the Medical College of Georgiaat Augusta University.

The new IMMCG, codirected by Georgia Research Alliance Eminent Scholars Catherine Lynn Hedrick, PhD, and Klaus Ley, MD, who joined the MCG at Augusta University faculty late last summer, focuses on better understanding the immune systems seemingly diametric roles in enabling good health and in contributing to major killers like cancer and heart disease.

The first recruits bring to MCG more immunological strength in major areas of research and clinical expertise of the medical school, says Hedrick.

Already onboard is Kunzhe Dong, PhD, a vascular immunologist with expertise in long noncoding RNA, literally long RNAs which regulate gene activity both up and down. He was first author on a 2022 study showing that a long noncoding RNA called CARMN is found in abundance in the healthy smooth muscle cells that give our blood vessels strength and flexibility and is significantly decreased in atherosclerosis. The finding provided more insight into how blood vessel disease happens as it pointed toward new ways to treat it. He also has studied autophagy, a fundamental the immune system uses to eliminate invading microorganisms and cell debris by ingesting them, and novel methods for protecting against destructive inflammation prompted by infection and by vascular disease.

Dong earned his PhD in animal genetics, breeding and reproduction from the Chinese Academy of Agricultural Sciences in Beijing, came to MCG in 2017 as a postdoctoral fellow studying with Vascular Biologist Jiliang Zhou, PhD, in the Department of Pharmacology and Toxicology, and was promoted to senior postdoctoral fellow in 2021. He received an American Heart Association Career Development Award in 2022, which runs through 2025, as well as an AHA Postdoctoral Fellowship during his training. Dong also received a 2022 travel grant for early career investigators from the AHA journal Arteriosclerosis, Thrombosis and Vascular Biology.

Marco Orecchioni, PhD, an immunologist and cellular biologist, who studied with Ley at the La Jolla Institute for Immunology in California, will be joining the IMMCG faculty May 1. The Italy native earned his PhD from the University of Sassari, before moving to La Jolla as a postdoctoral fellow in 2017. He was promoted to instructor in 2022.

Orecchionis work includes elucidating the role of olfactory (smell) receptors on macrophages, immune cells that can turn inflammation both up and down and can also consume cellular debris. He is working to better understand how these receptors, which seem to be more common in disease states like arteriosclerosis, affect immune cells, including driving inflammation, and whether they provide an unexplored connection between diet and the progression of heart disease and other metabolic problems. His research in collaboration with Ley and Hedrick has been published in top-tier journals including Science. A focus has been the simple chemical octanal which is detected by the olfactory receptors, and their connection prompts production of proinflammatory factors. The scientists have found levels of octanal in human and mouse blood sufficient to activate the respective receptors. When they boost octanal levels, they have found it increases characteristic plaque in blood vessels, and when they genetically delete the receptor it reduces disease, findings that point toward the smell receptor as both a sound prevention and treatment target. They also are exploring the possibility that octanal has effects in other diseases like cancer. Hedrick notes that despite the common ground of inflammation in the major killers of cancer and cardiovascular disease, they have two different environments with different inflammation types.

Orecchioni received an AHA Career Development Award in 2022 that continues today and received the Conrad Prebys Foundation Award in 2021. The foundation supports arts, medical research, health care and youth success in the San Diego community. He also received an AHA postdoctoral fellowship in 2018 and is associate editor of Frontiers in Immunology.

Also starting May 1 is Yanfang Peipei Zhu, PhD, a cancer immunologist coming to MCG and the IMMCG from the University of California San Diego. Zhu completed her postdoctoral fellowship at the La Jolla Institute for Immunology with Hedrick and was named an instructor at the institution before moving to the UCSD in 2020. Her research focus is neutrophils, short-lived immune cells that are early arrivers when we get a bacterial or viral infection. Their levels can shrink in response to problems like stress, as well as congenital or later problems that affect their production in the bone marrow. Zhus lab identified a progenitor cell called NeP that just makes neutrophils and a similar one called hNeP, in both mouse and human bone marrow. They also found that when cancer is present, these progenitor cells go right to the site of the tumor to support its growth. Now they are looking to better categorize which neutrophils and NePs support a healthy immune response versus cancer with the goal of identifying new biomarkers and treatment targets. Zhu also is exploring the cells potential role in atherosclerosis. Additionally, she is an expert in next-generation sequencing technologies that enable high throughput examination of the fine details of the genome.

Zhu earned her PhD from the University of Louisville School of Medicine in Kentucky before going to the Hedrick lab for her postdoc work, where she received a National Cancer Institute scholarship. She is academic editor for the Journal of Cellular Immunology and an editor for The Journal of Immunology and Microbiology.

Rafael S. Czepielewski, PhD, joins IMMCG July 1 from Washington University Medical School in Saint Louis, Missouri, one of the nations top immunology programs. The mucosal immunologists research focus is better understanding inflammatory bowel disease, or IBD, and changes to the lymphatic system during the course of the disease. The lymphatic system is part of the immune system defined as the tissues and organs that produce, store and carry white blood cells throughout the body where they patrol for infections and other invaders. IBD, which includes Crohns disease and ulcerative colitis, are both risk factors for colon cancer. Last year, Czepielewski received a Career Development Award from the Crohns & Colitis Foundation for his work on how crosstalk between the lymphatic vessels, microvessels throughout the body that carry lymph (fluid) away from tissues, and immune cells control IBD. His discoveries include little nests of immune cells along the lymphatic system in IBD, and now he and his new colleagues want to answer questions like how they got there and what they are doing.

Czepielewski received a Young Investigator Award from the 2021 Lymphatic Forum , a biennial event where researchers worldwide present and discuss studies of lymphatics in health and disease. Additionally, he is a fantastic microscopist, Hedrick says, in his case, that includes expertise in intravital microscopy, where you can look at more than one biological process at a time in living research animals, like transparent roundworms called C. elegans.

He earned his PhD from Brazils Pontificia Universidade Catlica do Rio Grande do Sul and joined the faculty as an instructor in 2021. During his PhD work he completed an international PhD fellowship at the Immunology Institute of the Icahn School of Medicine at Mount Sinai in New York City.

Adil Rasheed, PhD, a postdoctoral fellow completing his studies in vascular immunology at the University of Ottawa Heart Institute in Ontario, will start at IMMCG Sept. 11. At the Heart Institute, Rasheed has been honored for his leadership in postdoctoral studies and as the Ottawa Regions Cardiovascular Trainee of the Year. He is a member of the American Heart Association journal Arteriosclerosis, Thrombosis and Vascular Biology Early Career Editorial Board. He was a founding member of the online community Trainees in Metabolism, which hosted seminars and workshops on a range of relevant topics like effective mentorship and scientific communication.

Rasheed will bring with him studies of the protein MLKL, a protein known to play a key role in programmed cell death and which at high levels is associated with inflammatory bowel disease in children. He is finding MLKLs role in cell death appears to be a factor in accumulation of lipid and other substances inside blood vessels in atherosclerosis, and the protein has a significant role as an immune regulator in blood vessel and possibly other metabolic diseases. Rasheed also has an interest in the development of immune cells in the bone marrow, called hematopoiesis. He is the 2022 recipient of the Young Investigator Award from the journal STEM CELLS Translational Medicine for his pioneering research in heart disease while still working on his PhD at the University of Toronto.

LikeLoveHahaWowSadAngry

See original here:
Immunology Center of Georgia recruits reflect expertise from ... - Jagwire Augusta

FDA Fast Tracks BCMA-Targeted CAR T-Cell Therapy for R/R … – AJMC.com Managed Markets Network

A version of this article was originally published on OncLive. This version has been lightly edited.

The FDA has granted a fast track designation to CB-011, a CRISPR-edited allogeneic chimeric antigen receptor (CAR) T-cell therapy developed by Caribou Biosciences, for the treatment of patients with relapsed/refractory multiple myeloma.1

CB-011 targets the B-cell maturation antigen (BCMA). This is the first allogeneic anti-BCMA CAR T-cell therapy engineered to improve duration of antitumor response through an immune cloaking, genome-editing approach that removes the B2M protein and inserts a B2MHLA-E fusion protein, according to the company.2

In November 2022, the FDA cleared an Investigational New Drug application for CB-011.2 Now, the product is under evaluation in the multicenter, open-label study CaMMouflage trial (NCT05722418).3,4

Fast Track designation for CB-011 allows us instrumental interactions with the FDA as we progress our clinical development and regulatory plans for CB-011, Syed Rizvi, MD, chief medical officer at Caribou Biosciences, stated in a press release.1 This designation could not be [timelier,] as we recently dosed our first patient in the phase 1 CaMMouflage trial.

The CaMMouflage trial will include patients who have received at least 3 prior lines of therapy. Eligible patients are also required to have an ECOG performance status of 0 or 1 and to have adequate hematologic, renal, hepatic, pulmonary, and cardiac function.3

Patients who have received a BCMA-targeted therapy within 3 months of enrollment and/or any prior CAR T-cell therapy are excluded. Those who received autologous stem cell transplant within 6 weeks of lymphodepletion or allogeneic stem cell transplant within 6 months of lymphodepletion, who have an active or prior history of central nervous system involvement, or who have received a live, attenuated vaccine with 4 weeks of lymphodepletion are not eligible.3

In the part A, the escalation stage of the trial, investigators will assess ascending doses of CB-011 in combination with cyclophosphamide and fludarabine to establish the recommended phase 2 dose (RP2D) of the regimen in a standard 3+3 dose-escalation design. For part B, the expansion stage, investigators will assess responses to the RP2D, or the maximum tolerated dose as measured by International Myeloma Working Group criteria.3

Recruitment for CaMMouflage is ongoing. Caribou shared plans to assign patients to a single administration of CB-011 at a dose of 50 x 106 CAR T cells this year.1

Cas12a CRISPR hybrid RNA-DNA (chRDNA) technology was utilized to make 4 gene edits in the creation of CB-011. In edits 1 and 2, investigators target cancer cells by site-specifically inserting a humanized anti-BCMA CAR into the TRAC gene. This mechanism knocks out T cell receptor expression, thereby reducing the risk for graft-vs-host disease (GVHD).2

In edits 3 and 4, investigators prevent recognition and rejection by patient T cells and blunt rejection by natural killer (NK) cells by site-specifically inserting a B2MHLA-E peptide fusion gene into the B2M gene of the CAR T cells. These edits disable endogenous B2M expression, which eliminates endogenous HLA class I presentation and reduces T cell-mediated rejection. At the same time, these changes facilitate expression of B2MHLA-E which reduces rejection caused by NK cells.2

Prior preclinical findings presented at the 2022 AACR Annual Meeting indicated that the CAR T cells expressing the B2M-HLA-E fusion induced a survival benefit compared with cells that do not express the fusion in the presence of NK cells in vitro.4 This result suggests that these cells may be able to fight off a recipients NK cells and circulate longer.

Furthermore, CB-011 induced long-term survival in mice carrying established orthotopically-engrafted multiple myeloma cells. Mice who received high doses of CB-011 also appeared to avoid GVHD.4

Our goal is to develop CB-011 as a readily available off-the-shelf treatment option for patients with relapsed or refractory multiple myeloma to overcome the need for apheresis or bridging therapy, variable quality and long manufacturing timelines, manufacturing failures, or the inability to bear the burden of treatments that require frequent dosing over several months, Rizvi added in the press release.1

CB-011 is Caribous second allogeneic CAR T-cell agent that is under exploration in hematologic malignancies.

Investigators are assessing CB-010, a CAR T-cell therapy with a PD-1 knockout, in patients with relapsed or refractory B cell non-Hodgkin lymphoma as part of the ongoing phase 1 ANTLER trial NCT04637763).2 One patient in that trial who received 8 prior lines of systemic therapy had an ongoing complete response through month 15.5

References

1. Caribou Biosciences announces FDA granted fast track designation to CB-011, an allogeneic CAR-T cell therapy for relapsed or refractory multiple myeloma. News release. Caribou Biosciences. April 4, 2023. Accessed April 6, 2023. https://investor.cariboubio.com/

2. Caribou Biosciences announces FDA clearance of IND application for CB-011, an allogeneic anti-BCMA CAR-T Cell therapy for the treatment of relapsed or refractory multiple myeloma. News release. Caribou Biosciences. November 21, 2022. Accessed April 6, 2023. https://investor.cariboubio.com/news-releases/

3. CRISPR-edited allogeneic anti-BCMA CAR-T cell therapy in patients with relapsed/refractory multiple myeloma (CaMMouflage). Updated March 2, 10, 2023. Accessed April 6, 2023. https://www.clinicaltrials.gov/ct2/show/NCT05722418

4. Garner E, Degagne E, Roy S, et al. A BCMA-specific allogeneic CAR-T cell therapy (CB-011) genome-engineered to express an HLA-E fusion transgene to prevent immune cell rejection. Cancer Res. 2022;82(suppl 12):LB009. doi:10.1158/1538-7445.AM2022-LB009

5. CRISPR-edited allogeneic anti-CD19 CAR-t cell therapy with PD-1 knockout induces prolonged complete response in relapsed/refractory follicular lymphoma patient: case report from CB-010 ANTLER trial. Presented at: the Lymphoma, Leukemia, & Myeloma Congress; New York, NY; October 18-22, 2022.

Go here to read the rest:
FDA Fast Tracks BCMA-Targeted CAR T-Cell Therapy for R/R ... - AJMC.com Managed Markets Network

Bazedoxifene and cholecalciferol | DDDT – Dove Medical Press

Introduction

Osteoporosis is a skeletal disorder characterized by low bone mass and an increased risk of bone fracture. Bone mass reaches its peak in young adulthood, and increased bone resorption relative to bone formation leads to the lowering of bone mass. According to the World Health Organization, osteoporosis is defined as hip or lumbar spine bone marrow density of more than 2.5 standard deviations below the mean found in the young-adult population.1 Osteoporosis is a significant public health concern among the elderly due to the increased morbidity and mortality associated with bone fractures. It affects both sexes and all races, and its prevalence is expected to rise as the global population continues to age.1

The pharmacologic agents for the prevention and treatment of osteoporosis include calcium, vitamin D, bisphosphonates, calcitonin, estrogen, selective estrogen receptor modulator (SERM), parathyroid hormone, and anti-receptor activator of nuclear factor-kappa B ligandantibody (denosumab).2 The therapeutic potential of new treatment approaches, such as exosomes derived from endothelial cells or mesenchymal stem cells, has been investigated recently in animal models.3,4

Bazedoxifene, a third-generation SERM, exhibits tissue-selective action, functioning as an agonist in skeletal tissue but as an antagonist in breast and uterine tissues.5,6 Bazedoxifene has been approved for the treatment of postmenopausal osteoporosis by the European Medicines Agency, and conjugated estrogens/bazedoxifene have been approved for the prevention of postmenopausal osteoporosis by the United States Food and Drug Administration.7,8 Cholecalciferol, commonly known as vitamin D3, plays an important role in bone metabolism. Cholecalciferol is converted to calcifediol (25-hydroxycholecalciferol) in the liver and then to calcitriol (1,25-dihydroxycholecalciferol), the active form of vitamin D, in the kidney. Although vitamin D can be obtained from dietary intake and synthesized in the skin after exposure to sunlight, its deficiency is common. The National Osteoporosis Foundation recommends 8001000 IU of vitamin D intake per day for individuals aged 50 and older.1

A fixed-dose combination formulation of bazedoxifene and cholecalciferol is a potentially promising therapeutic option for postmenopausal osteoporosis patients as it can improve treatment efficacy and medication compliance. Before developing a fixed-dose combination formulation, the pharmacokinetic (PK) interactions between bazedoxifene and cholecalciferol need to be assessed. This study aimed to examine the PK interactions between these drugs as well as their safety and tolerability when co-administered in healthy male subjects.

The study was designed as an open-label, randomized, three-period, three-treatment, six-sequence, crossover clinical trial. Healthy male volunteers aged between 19 and 40 years with body mass index (BMI) between 19 and 28 kg/m2 were eligible for inclusion. Subjects were screened based on past medical history, physical examination including vital signs (blood pressure, heart rate, and body temperature), urine drug screening, clinical laboratory tests, serology tests, and 12-lead electrocardiogram (ECG). Subjects with a history of venous thromboembolism, hypercalciuria, renal stone, hepatobiliary disease, galactose intolerance, drug abuse, or clinically significant hypersensitivity reaction were excluded.

A total of 30 subjects were randomly assigned to six sequences comprised of three treatments: one tablet of 20 mg bazedoxifene (Viviant; Pfizer Ltd., Seoul, Korea), two tablets of 800 IU cholecalciferol (HGP1501; Hanmi Pharmaceutical Co. Ltd., Seoul, Korea), or one tablet of 20 mg bazedoxifene along with two tablets of 800 IU cholecalciferol (Table 1). Outpatient visits were scheduled on day 10 of period 1 and day 9 of periods 2 and 3. At that time, subjects were provided with sunscreens (sun protection factor 50) and diaries to record their diet and activity. Subjects were asked to limit their exposure to sunlight by applying sunscreen and covering themselves with clothes and hats for outdoor activities. Subjects were required to refrain from taking dietary supplements and foods high in vitamin D content. Between two consecutive periods, there was a washout period of at least 14 days. These subjects were admitted to the Clinical Trial Center at Asan Medical Center (Seoul, Korea) the day before drug administration. The test drugs were administered orally under fasting conditions with 150 mL of water. After receiving the investigational drug(s), subjects were required to fast for four hours. Depending on the treatment, subjects were discharged on either day 2 (bazedoxifene monotherapy) or day 6 (cholecalciferol monotherapy or combined therapy). A follow-up visit was scheduled two weeks after the last dose.

Table 1 Overall Study Design

To determine the plasma bazedoxifene concentration, serial blood samples were collected at 0 (pre-dose), 1, 1.5, 2, 3, 4, 5, 6, 8, 10, 12, 14, 24, 48, 72, 96, and 120 hours after the dosing. To measure the baseline cholecalciferol level, blood samples were collected at 16, 12, 8, and 0 hours before the cholecalciferol dosing, and the average concentration for each individual was used as the baseline cholecalciferol concentration. Baseline-adjusted cholecalciferol concentrations were obtained by subtracting the baseline from the post-dose plasma cholecalciferol concentrations measured at 1, 1.5, 2, 3, 4, 5, 6, 8, 10, 12, 14, 16, 24, 48, 72, 96 and 120 hours after the treatment. If the baseline-adjusted cholecalciferol concentration had a negative value, zero was assigned.

Blood samples used for the drug concentration measurements were drawn into ethylenediaminetetraacetic acid K2 tubes. Plasma was separated by centrifugation at 1800 g for 8 minutes at 4 C and stored in Eppendorf tubes at 70 C until analysis. At the analytical laboratory (BioCore Co. Ltd., Seoul, Korea), samples were thawed at room temperature. The plasma concentrations of bazedoxifene and cholecalciferol were assayed using validated liquid chromatography with tandem mass spectrometry (LC-MS/MS). Bazedoxifene samples were prepared by liquid-liquid extraction, and cholecalciferol samples by protein precipitation and solid-phase extraction. Liquid chromatography was conducted using a Shimadzu UFLC system (Shimadzu Corp., Kyoto, Japan). For tandem mass spectrometry, a SCIEX TQ5500 mass spectrometer (AB Sciex LLC, MA, USA) was used. The calibration curves covered the ranges of 0.120 ng/mL for bazedoxifene and 0.110 ng/mL for cholecalciferol. For bazedoxifene, the accuracy of LC-MS/MS was 91.8113.0%, and the precision was 0.15.5%. For cholecalciferol, the accuracy of LC-MS/MS was 92.7105.6%, and the precision was 0.24.5%. The lower limit of quantification was 0.1 ng/mL for both compounds.

The study protocol was approved by the Institutional Review Board (IRB) of Asan Medical Center (IRB number: 20170227) and by the Korean Ministry of Food and Drug Safety. The study was registered at ClinicalTrials.gov (NCT03089112). All subjects provided written informed consent before receiving screening tests. All study procedures were conducted in accordance with the ethical principles stated in the Declaration of Helsinki and by the Good Clinical Practice Guidelines of the International Council for Harmonisation.9,10 The study was conducted from March 31, 2017 to June 16, 2017.

The PK parameters of bazedoxifene and cholecalciferol in each subject were analyzed by the non-compartmental method using Phoenix WinNonlin version 6.4 (Certara, NJ, USA). This analysis was based on the actual sampling time. The maximum plasma concentration (Cmax) and the time to reach Cmax (Tmax) were determined from the observed values. The terminal elimination rate constant (z) was estimated by linear regression analysis of the terminal portion of the semilogarithmic concentration-time curve. The terminal elimination half-life (t1/2) was calculated as the natural log of two divided by z. Demographic data and PK parameters were summarized using descriptive statistics. The Cmax and the values for the area under the plasma concentration-time curve from time zero to the last quantifiable concentration (AUClast) were log-transformed to compare the drug exposure between the combined therapy and monotherapy. The point estimate and 90% confidence interval (CI) for the geometric mean ratio (GMR) of the combined therapy to monotherapy were obtained for Cmax and AUClast.

Safety and tolerability were assessed throughout the study by physical examinations, laboratory tests (complete blood count, blood chemistry, and urinalysis), 12-lead ECG, and monitoring of adverse events (AEs). AEs were coded according to the Medical Dictionary for Regulatory Activities (MedDRA version 19.1) and recorded in terms of symptom/sign, onset, duration, severity, relationship to the investigational drug(s), action taken, and outcome.

Of the 30 study participants who received the investigational drug(s) at least once, 27 subjects completed the study (Figure 1). Two subjects withdrew their consent to participate, and one subject was excluded at the investigators discretion due to a medical need for concomitant medication that could potentially affect the PK data. Participant demographics, including age, weight, height, and BMI, are summarized in Table 2. The mean standard deviation (SD) values were 28.63 4.18 years for age, 71.53 6.99 kg for weight, 173.55 4.80 cm for height, and 23.75 2.09 kg/m2 for BMI. All subjects who received the investigational drug(s) at least once were included in the safety and tolerability assessment.

Table 2 Demographic Characteristics of the Participants (n=30)

Figure 1 Subject disposition.

The 27 subjects who completed the study were included in the PK analysis set, and the PK parameters are presented in Table 3. For bazedoxifene, the Cmax values (mean SD) for monotherapy and combined therapy were 3.30 0.92 ng/mL and 3.62 1.39 ng/mL, respectively. The AUClast values (mean SD) for monotherapy and combined therapy were 44.32 22.24 hng/mL and 50.78 24.98 hng/mL, respectively. The mean plasma concentration-time profiles of bazedoxifene for monotherapy and combined therapy nearly overlapped (Figure 2A). For bazedoxifene, the GMR (90% CI) of the combined therapy to monotherapy was 1.044 (0.92631.1765) for Cmax and 1.1329 (1.02321.2544) for AUClast (Table 4).

Table 3 Pharmacokinetic Parameters of Bazedoxifene and Baseline-Adjusted Cholecalciferol in Healthy Male Subjects (n=27)

Table 4 Geometric Mean Ratios of Combined Therapy to Monotherapy for AUClast and Cmax

Figure 2 Mean plasma concentration-time curves: (A) bazedoxifene (B) baseline-adjusted cholecalciferol. The error bars denote standard deviations.

For baseline-adjusted cholecalciferol, the Cmax values (mean SD) for monotherapy and combined therapy were 2.25 0.47 ng/mL and 1.95 0.54 ng/mL, respectively. The AUClast values (mean SD) for monotherapy and combined therapy were 59.43 22.95 hng/mL and 49.18 24.40 hng/mL, respectively. The mean plasma concentration-time profiles of baseline-adjusted cholecalciferol for monotherapy and combined therapy are shown in Figure 2B. For baseline-adjusted cholecalciferol, the GMR (90% CI) of combined therapy to monotherapy was 0.8543 (0.80050.9117) for Cmax and 0.8056 (0.74450.8717) for AUClast (Table 4).

Seventeen subjects showed a total of 26 AEs after drug administration (Table 5). No serious AE occurred throughout the entire study. All AEs were mild in severity and resolved without any sequelae. The most common AE was nasopharyngitis (five events in five subjects). Clinically significant findings from the physical examination were phlebitis of the arm and venipuncture site bruise. Clinically significant laboratory abnormalities included increased blood levels of creatine phosphokinase and triglyceride and decreased blood levels of neutrophil count. No clinically significant abnormalities were found with respect to vital signs and 12-lead ECG. Twenty-five AEs were considered to have no or unlikely relationship with the investigational drugs. One AE, fatigue observed after combined therapy, was considered to have a possible relationship with the administered drugs.

Table 5 Adverse Events in the Study Population After Drug Administration

This study investigated the PK characteristics of bazedoxifene and cholecalciferol, their PK interactions, and the safety and tolerability of combined therapy with these drugs in healthy male subjects.

The terminal elimination half-life of bazedoxifene was approximately 27 hours, and that of cholecalciferol was 13 hours in our study. The washout period of 14 days should therefore have been sufficient for both investigational drugs to be fully eliminated by the next period. The blood samples obtained up to 120 hours after dosing provided sufficient information for characterizing the exposures to bazedoxifene and cholecalciferol.

Previous studies on bazedoxifene pharmacokinetics have indicated a Tmax of 12 hours and a half-life of approximately 28 hours.11 As shown in Figure 2 and Table 3, bazedoxifene was rapidly absorbed when administered alone or in combination with cholecalciferol, showing median Tmax values of 2.00 h and 1.53 h, respectively. The Tmax of cholecalciferol is known to be approximately 15 hours. In our study, the median Tmax of cholecalciferol was 11.98 h when administered alone, similar to the 12.00 h value found for its co-administration with bazedoxifene.

In a recent study on bazedoxifene, the mean Cmax and AUClast in healthy male subjects after a single 20 mg oral dose were 3.191 ng/mL and 44.697 hng/mL, respectively.12 These numbers are consistent with the results of the current study (3.30 ng/mL and 44.32 hng/mL). The PK parameters Cmax and AUClast were used in our analyses to compare the combined therapy and monotherapy exposures. With bazedoxifene, the 90% CI for the GMR of the combined therapy to bazedoxifene monotherapy for Cmax fell within the 0.801.25 range, and for AUClast it was nearly within the above-mentioned range.

In the case of cholecalciferol, the AUClast was lower when this drug was co-administered with bazedoxifene, as indicated by the GMR of 0.8056 and associated 90% CI of 0.74450.8717. Bazedoxifene and cholecalciferol are drugs that exhibit wide therapeutic ranges.1315 Cholecalciferol is known to reach a sigmoidal dose-response curve plateau at a dose of 600 IU.15 Hence, based on the GMRs observed in our exploratory study, the difference in the AUClast for cholecalciferol is unlikely to have clinical significance in treatment efficacy at the dose level used in our protocol.

All of the AEs observed in our study population were mild, and the frequency of AEs in subjects who received combined therapy was not significantly different from that in subjects who received monotherapy. The most common AE observed in our present trial cohort was nasopharyngitis, which we considered unrelated to the investigational drugs.

One limitation of the present study was that the participants were all healthy men. The study was exploratory in nature, and male subjects were included to facilitate enrollment and minimize health risks to subjects. Drug-drug interaction studies are often conducted with male subjects, and the results are applied to women as well as men because gender does not seem to affect the pattern of drug-drug interaction for many drugs. Assuming that the PK interactions would follow the same pattern in men and women, this study was conducted in men instead of women. Additional studies in postmenopausal women with osteoporosis and patients with different pathophysiological conditions will help further characterize the PK interactions between bazedoxifene and cholecalciferol.

The combined therapy of 20 mg bazedoxifene (one tablet) and 1600 IU cholecalciferol (two tablets of 800 IU) was safe and well tolerated in healthy male subjects. In this present study, the oral co-administration of bazedoxifene with cholecalciferol tended to decrease the cholecalciferol exposure slightly. Considering that both drugs have wide therapeutic ranges, dose adjustment of cholecalciferol may not be necessary for its co-administration with bazedoxifene.

AE, adverse event; AUClast, area under the concentration-time curve from time zero to the last quantifiable concentration; BMI, body mass index; CI, confidence interval; Cmax, maximum plasma concentration; ECG, electrocardiogram; GMR, geometric mean ratio; IRB, Institutional Review Board; LC-MS/MS, liquid chromatography with tandem mass spectrometry; z, terminal elimination rate constant; PK, pharmacokinetic; SD, standard deviation; SERM, selective estrogen receptor modulator; Tmax, time to reach Cmax; t1/2, terminal elimination half-life.

The authors do not intend to share individual de-identified participant data of this study due to confidentiality.

This study was sponsored by Hanmi Pharmaceutical Co. Ltd.

Hyeong-Seok Lim has received grants from Hanmi Pharmaceutical Co. Ltd. for a range of research projects, including the study reported in this article. Jina Jung and Sung Hee Hong are employees of Hanmi Pharmaceutical Co. Ltd. The remaining authors declare no competing interests in relation to this article.

1. Cosman F, de Beur SJ, LeBoff MS, et al. National Osteoporosis Foundation. Clinicians guide to prevention and treatment of osteoporosis. Osteoporos Int. 2014;25(10):23592381. doi:10.1007/s00198-014-2794-2

2. Rejnmark L, Mosekilde L. New and emerging antiresorptive treatments in osteoporosis. Curr Drug Saf. 2011;6(2):7588. doi:10.2174/157488611795684686

3. Song H, Li X, Zhao Z, et al. Reversal of osteoporotic activity by endothelial cell-secreted bone targeting and biocompatible exosomes. Nano Lett. 2019;19(5):30403048. doi:10.1021/acs.nanolett.9b00287

4. Zeng ZL, Xie H. Mesenchymal stem cell-derived extracellular vesicles: a possible therapeutic strategy for orthopaedic diseases: a narrative review. Biomater Transl. 2022;3(3):175187. doi:10.12336/biomatertransl.2022.03.002

5. Komm BS, Kharode YP, Bodine PV, Harris HA, Miller CP, Lyttle CR. Bazedoxifene acetate: a selective estrogen receptor modulator with improved selectivity. Endocrinology. 2005;146(9):39994008. doi:10.1210/en.2005-0030

6. Stump AL, Kelley KW, Wensel TM. Bazedoxifene: a third-generation selective estrogen receptor modulator for treatment of postmenopausal osteoporosis. Ann Pharmacother. 2007;41(5):833839. doi:10.1345/aph.1H428

7. Conbriza. European medicines agency; 2009. Available from: https://www.ema.europa.eu/en/medicines/human/EPAR/conbriza. Accessed October 21, 2022.

8. DUAVEE. Drug Label (NDA 022247). Silver Spring, MD: US Food and Drug Administration; 2013.

9. World Medical Association. World medical association declaration of Helsinki: ethical principles for medical research involving human subjects. JAMA. 2013;310(20):21912194. doi:10.1001/jama.2013.281053

10. Guideline for Good Clinical Practice E6(R2). International council for harmonisation of technical requirements for pharmaceuticals for human use; 2016. Available from: https://database.ich.org/sites/default/files/E6_R2_Addendum.pdf. Accessed October 21, 2022.

11. Gatti D, Rossini M, Sblendorio I, Lello S. Pharmacokinetic evaluation of bazedoxifene for the treatment of osteoporosis. Expert Opin Drug Metab Toxicol. 2013;9(7):883892. doi:10.1517/17425255.2013.794221

12. Yeun JS, Kan HS, Lee M, et al. Pharmacokinetic comparison of two bazedoxifene acetate 20 mg tablet formulations in healthy Korean male volunteers. Transl Clin Pharmacol. 2020;28(2):102108. doi:10.12793/tcp.2020.28.e7

13. Archer DF, Pinkerton JV, Utian WH, et al. Bazedoxifene, a selective estrogen receptor modulator: effects on the endometrium, ovaries, and breast from a randomized controlled trial in osteoporotic postmenopausal women. Menopause. 2009;16(6):11091115. doi:10.1097/gme.0b013e3181a818db

14. Kawate H, Takayanagi R. Efficacy and safety of bazedoxifene for postmenopausal osteoporosis. Clin Interv Aging. 2011;6:151160. doi:10.2147/CIA.S15711

15. Institute of Medicine. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: The National Academies Press; 2011.

Read the original here:
Bazedoxifene and cholecalciferol | DDDT - Dove Medical Press