Cord Stem Cell Banking Market to Influence the Value of USD 45.64 Billion by 2030 – openPR

Cord Stem Cell Banking Market

Get Full Report: https://www.databridgemarketresearch.com/reports/global-cord-stem-cell-banking-market

Data Bridge Market Research analyses that the cord stem cell banking market, which was USD 9.3 billion in 2022, would rise up to USD 45.64 billion by 2030 and is expected to undergo a CAGR of 22% during the forecast period 2023 to 2030. In addition to the insights on market scenarios such as market value, growth rate, segmentation, geographical coverage, and major players, the market reports curated by the Data Bridge Market Research also include depth expert analysis, patient epidemiology, pipeline analysis, pricing analysis, and regulatory framework.

The cord stem cell banking market is analyzed and market size insights and trends are provided by storage type, product type, service type, source, and indication as referenced above.

The countries covered in the cord stem cell banking market report are U.S., Canada, and Mexico in North America, Germany, France, U.K., Netherlands, Switzerland, Belgium, Russia, Italy, Spain, Turkey, Rest of Europe in Europe, China, Japan, India, South Korea, Singapore, Malaysia, Australia, Thailand, Indonesia, Philippines, Rest of Asia-Pacific (APAC) in the Asia-Pacific (APAC), Saudi Arabia, U.A.E, South Africa, Egypt, Israel, Rest of Middle East and Africa (MEA) as a part of Middle East and Africa (MEA), Brazil, Argentina and Rest of South America as part of South America.

North America dominates the cord stem cell banking market due to an increase in the presence of major market players in the U.S., ongoing approval of stem cell lines for disease treatment, and growing awareness among the population in this region.

Asia-Pacific is expected to witness significant growth due to a rise in the elderly population, an increase in the incidence of chronic diseases, and growing per capita healthcare expenditure in this region. Also, the developing healthcare infrastructure within the region is boosting market growth.

The cord stem cell banking market competitive landscape provides details by competitor. Details included are company overview, company financials, revenue generated, market potential, investment in research and development, new market initiatives, global presence, production sites and facilities, production capacities, company strengths and weaknesses, product launch, product width and breadth, application dominance. The above data points provided are only related to the companies' focus related to cord stem cell banking market.

Some of the major players operating in the cord stem cell banking market are:

CBR Systems, Inc., (U.S.) Cordlife (Singapore)Cryo-Cell International, Inc., (U.S.)ViaCord (U.S.)Cryo-Save (Netherlands)LifeCell International Pvt. Ltd. (India)StemCyte India Therapeutics Pvt. Ltd (U.S.)Global Cord Blood Corporation (China)Smart Cells International Limited (U.K.)Vita 34 1997 - 2023, Inc (Germany)Lisata Therapeutics, 2023 (U.S.)BrainStorm Cell Limited (U.S.)Regrow Biosciences Pvt. Ltd. (India)

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Cord Stem Cell Banking Market to Reach USD 45.64 Billion, with an Excellent CAGR of 22% by 2030

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Cord Stem Cell Banking Market to Influence the Value of USD 45.64 Billion by 2030 - openPR

Scientists Enhance New Neurons to Restore Memory, Elevate Mood … – UNC Health and UNC School of Medicine

The lab of Juan Song, PhD, and colleagues at the UNC School of Medicine, demonstrated the therapeutic potential of new neurons generated in adulthood for modulating the pathology and functional deficits associated with Alzheimers disease using rodent models.

CHAPEL HILL, NC In adult human brains, the hippocampus generates new neurons (adult-born neurons, or ABNs) throughout life, helping us maintain memories and regulate emotions. Scientists call this process adult hippocampus neurogenesis (AHN). In people with Alzheimers disease (AD), this process is impaired, leading to reduced production of ABNs with poorer qualities. Given that AD patients often develop both cognitive symptoms (such as memory loss) and non-cognitive symptoms (such as anxiety and depression) for which AHN plays a critical role, one way to help Alzheimers patients achieve symptom relief could be to restore AHN.

Published in the journal Cell Stem Cell, research from UNC School of Medicine scientists demonstrated that stimulating a brain region called Supramammilary nucleus (SuM) located in the hypothalamus effectively enhanced adult-born neurons in the otherwise impaired Alzheimers brains of mice. After patterned stimulation of SuM, AD brains developed more ABNs with improved qualities. Importantly, activation of these SuM-modified ABNs restored both cognitive and affective deficits in AD mouse models.

Its been a longstanding question whether AHN can be sufficiently enhanced in impaired AD brains to improve brain function, said senior author Juan Song, PhD, associate professor of pharmacology and a Jeffrey Houpt Distinguished Investigator at the UNC School of Medicine. An important point to consider when addressing these questions is the low-level hippocampal neurogenesis, which becomes even lower in AD patients.

By manipulating a small number of ABNs in the AD brain, we demonstrate that ABNs can be enhanced even in the presence of AD pathology, and these enhanced ABNs are important for the restoration of behaviors and hippocampal function.

To enhance ABNs in AD brains, Song and colleagues adopted an elegant two-step ABN-enhancing strategy by first stimulating SuM using a patterned optogenetic paradigm with the goal of promoting the generation and developmental properties of ABNs, followed by stimulating the activity of SuM-enhanced ABNs using chemogenetics.

Optogenetics involves the use of light to alter the activity of brain cells expressing light-sensitive opsin genes. Chemogenetics involves the use of inert molecules to alter the activity of brain cells expressing designers receptors.

Interestingly, SuM stimulation alone or activation of ABNs without SuM stimulation failed to restore behavioral deficits in AD mice. Song said. These results suggest that multi-level enhancement of ABNs namely increasing their number, improving their developmental properties, and enhancing their activity is required to achieve their therapeutic benefits in AD brains.

When Song and colleagues further analyzed the protein changes in the hippocampus of AD mice in response to activation of SuM-enhanced ABNs, the researchers found that several well-known protein pathways were activated inside cells. These pathways include the ones important for synaptic plasticity of neuronal cells that allow enhanced communication among them, as well as the ones important for phagocytosis of non-neuronal microglia that allow efficient plaque clearance.

It is striking that multi-level enhancement of ABNs through combined SuM and ABN stimulations allows such a small number of ABNs make profound functional contribution in diseased AD brains, Song said. We are eager to find out the mechanisms underlying these beneficial effects mediated by activation of SuM-enhanced ABNs on AD pathology and hippocampal function. Future efforts will be needed to develop drugs that mimic these beneficial effects mediated by activation of SuM-enhanced ABNs. Ultimately, the hope is to develop first-in-class, highly targeted therapies to treat AD and related dementia.

The National Institutes of Health funded this research through grants R01MH111773, R01MH122692, RF1AG058160, R01NS104530 to Juan Song and R21AG071229, R01GM133107 to co-author Xian Chen, PhD, professor of biochemistry and biophysics at the UNC School of Medicine.

Co-first authors of the Cell Stem Cell paper are Ya-Dong Li and Yan-Jia Luo in the Song Lab. Other authors are, Ling Xie, Dalton Tart, Ryan N Sheehy, Libo Zhang, and Leon G Coleman Jr, all at the UNC School of Medicine.

Media contact: Mark Derewicz, 919-923-0959

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Scientists Enhance New Neurons to Restore Memory, Elevate Mood ... - UNC Health and UNC School of Medicine

Proliferation, not replication: HIV is lifelong because infected cells … – aidsmap

A poster and a talk both presented at the recent Conference on Retroviruses and Opportunistic Infections (CROI 2023) dampened down expectations that a cure for HIV may soon be possible using less risky and expensive methods than the stem-cell transplants that have so far cured five people (see this report for the latest).

Dr Natalie McMyn of Johns Hopkins University has found that, although during the first few years on antiretroviral therapy (ART) the number of cells capable of producing viable HIV (if ART is stopped) shrinks, in people taking ART continuously for a longer time, the size of this reservoir of virally-productive cells declines no more and may even slowly start to increase. The amount of cells withanyHIV DNA in them, whether productive or not, also stops declining after ten or so years on ART and may increase.

McMyns study is co-authored by several leaders in HIV cure research, including Professors Steven Deeks, Robert Siliciano and Janet Siciliano.

The HIV reservoir is a group of cells that are infected with HIV but have not produced new HIV (latent stage of infection) for many months or years. Latent HIV reservoirs are established during the earliest stage of HIV infection. Although antiretroviral therapycan reduce the level of HIV in the blood to an undetectable level, latent reservoirs of HIV continue to survive (a phenomenon called residual inflammation). Latently infected cells may be reawakened to begin actively reproducing HIV virions if antiretroviral therapy is stopped.

To eliminate a disease or a condition in an individual, or to fully restore health. A cure for HIV infection is one of the ultimate long-term goals of research today. It refers to a strategy or strategies that would eliminate HIV from a persons body, or permanently control the virus and render it unable to cause disease. A sterilising cure would completely eliminate the virus. A functional cure would suppress HIV viral load, keeping it below the level of detection without the use of ART. The virus would not be eliminated from the body but would be effectively controlled and prevented from causing any illness.

The chemical form in which HIV's genetic information is stored within infected cells.

The body's mechanisms for fighting infections and eradicating dysfunctional cells.

Its implications were explored ina talk given by Dr Jared Sternof Seattles Fred Hutch Cancer Institute at theCommunity Cure Workshop held the day before CROI opened.

Stern said that strategies aiming to cure HIV either by targeting cells for immune destruction (the shock and kill strategy) or by forcing them into permanent quiescence (the block and lock strategy) may not be sufficient in themselves to achieve a cure for HIV. A delicate, sequential balance of different strategies may be necessary.

The reason for the eventual stabilisation and even growth of the reservoir is that in the early years on ART, many cells remain that are capable of actively producing HIV viral particles. This is why the average viral load in people on ART is, at least initially, in the region of 2-4 copies per millilitre instead of zero.

When these cells do produce viable HIV, while they can infect new cells, they also become visible to the immune system. This both targets them for immune destruction, and sets them on the pathway towards apoptosis programmed cell death.

Later on however, cell division, rather than viral replication, becomes more important.Even the long-lived T-memory cells that form most of the viral reservoir have to divide now and then in order to replenish the bodys T-cells, often in response to infection. Because of this, later on, active viral production becomes rarer and the reservoir is mainly replenished by cell division.

When infected cells divide, they do not have to express HIV proteins or otherwise start the process of making virus they simply split, duplicating their DNA, including their HIV proviral DNA, as they do. These cells contain identical clones of HIV, because DNA has much less chance to mutate during cell division. This is called clonal expansion.

McMyns study involved 31 people who had been on fully-suppressive ART for a median time of nearly 23 years. All have maintained viral undetectability. Starting with CD4 counts of near-zero (this was the late 1990s), their median CD4 count rose to about 800 15 years after starting ART, but after that declined a little and plateaued at around 650.

The researchers took purified resting CD4 T-cells from each participants blood and did two tests. Firstly, they did a viral outgrowth assay. This measures the proportion of cells that can be induced to produce viral particles in the lab dish.

Previous investigations by Robert Siliciano in the early 2000s found a slow decrease in productive cells. He calculated that the HIV reservoir had a half-life of 44 months on ART, meaning the number of virally productive cells would halve in just over two years. This would mean that two per million resting CD4 cells being able to produce viable virus at baseline, that number would have gone down tenfold in 12 years and a hundredfold in 24.

This was not what they observed: the proportion of cells that were productively infected went down for the first 3-4 years on ART but then stopped decreasing and may even have increased very slightly since then.

The other test was a DNA assay of the cells, to detectallcells that contained lengths of proviral DNA. Because most of these are fragmentary or mutated and so cant produce virus, about 100 times as many CD4 T-cells contain proviral DNA than can produce viable virus. If the trend indicated by earlier studies continued, wed expect the proportion of cells containing HIV DNA to decline from 200 per million to two per million in 24 years too.

But the proviral DNA reservoir only declined in about the first nine years on ART and even then by not very much. After that it stayed steady or grew slightly and is now back to where it started in most of the participants studied. The proportion of DNA-containing cells that could produce viable virus was the same regardless of the amount of time on ART. The amount of DNA-containing cells and productively-infected cells differed by two orders of magnitude between the 31 individuals, but were correlated within individuals.

By successively diluting cell samples, the researchers genetically sequenced every DNA sequence in the CD4 resting T-cells they sampled in three individuals. From two of these people, viable virus could be produced from some samples, but not from the third persons cells. In this individual, virtually all viral isolates (DNA sequences) were genetically distinct from each other. Only three out of 44 sequences formed a pair with one of the other ones, indicating cloned DNA.

In the other two people, 19% of 59, and 36% of 97 proviral DNA sequences gave rise to fully replicating virus. In the first case, every single sequence that produced viable virus was identical, clearly originating from one single cell that had divided. There were three other clonal sequences that did not produce virus.

In the second case, 18 out of the 35 sequences that produced virus were identical, and three others almost identical. The other 14 productive sequences were, however, all different from each other apart from one pair, and there were 11 other clonal sequences that did not produce virus. These were mainly pairs and triads of identical sequences, but there was one clone of seven cells with identical DNA that was not productive.

Natalie McMyns main conclusion from her findings was that, while in some cases the HIV reservoir may stop being capable of producing new virus, in the large majority, cellular proliferation keeps the reservoir of cells containing viable virus topped up so we should not expect there to be too many people who can stop ART without their viral load bouncing back.

Jared Stern drew wider conclusions from this and related studies.

He said that as time goes by, the reservoir changes its nature under ART. Because active cells are cleared or self-destruct more quickly than inactive ones, over time the reservoir becomes less productive and more latent.

ART is good at preventing cells from becoming infected, he said. But its no good at stopping them staying infectious.

More latent means less likely to activate, but also less visible to the immune system which creates a dilemma for cure researchers. Should they attempt to activate more cells and alert the immune system, risking the danger of enlarging the reservoir with a new wave of cellular infections or should they try to maintain latency, even though in some people that means maintaining cells that will contain persistently viable viral DNA?

Essentially, people with HIV face a lottery during acute HIV infection. The virus' position of integration into a cells nucleus is rather random but it tends to pick sites nearest to the exterior of the nucleus, and these tend to be the areas where commonly active genes are being expressed. If HIV finds itself in a length of DNA that is rarely or never expressed the so-called gene deserts then even if the cell divides, it is unlikely ever to start producing virus.

On the other hand, if it is integrated into a gene that is often active, then it will likely be expressed when the gene activates. ART stops HIVs enzymes from getting very far into the process of producing viral components but it does not stop the cell dividing and cloning those potentially productive sequences.

This implies that before we can devise a safer and cheaper cure for HIV than wholesale replacement of the immune system, we need to answer some outstanding research questions we dont know the answer to.

What determines whether a cell becomes productive (and so dies) or latent (and therefore survives)? What determines that a cell switches from being latent to being productive? Why do some T-memory cells divide clonally and not others? Does HIV itself have a part to play in clonal expansion?

Should a cure make HIV less, or more, latent? Is long-term ART sufficient, at least in some proportion of people, to produce a deeply latent reservoir that cant rebound when ART is stopped? And how do we know who those people are?

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Proliferation, not replication: HIV is lifelong because infected cells ... - aidsmap

Trudy Oliver Tracks a Deadly, Shapeshifting Tumor – Duke University School of Medicine

Trudy Oliver, PhD, studies a type of cancer that has a 5-year overall survival rate of just 7%. Its biological drivers are different from most other cancers, so its harder to develop targeted treatments. On top of that, research into this tumor is under-funded.

Oliver, professor of pharmacology and cancer biology at Duke University School of Medicine, investigates small cell lung cancer, which is almost always linked to cigarette smoking. "Some people think 'Oh, you smoked. You got what you deserved. Why do we need to put money into this? she said.

Whatever you think about that statement, Olivers work suggests that it doesnt matter. Small cell lung cancer is a shapeshifter. Her recent research found that it evolves nimbly, changing identities in order to survive. Increasingly, scientists are finding that many cancers have this "plasticity" to some extent, especially when they are threatened by ever-more targeted treatments.

Because of that, small cell lung cancer has much more in common with other cancers than previously thought. "In order to understand how to treat any kind of cancer, we have to study them all," Oliver said.

Oliver joined the Duke faculty in July 2021 as a Duke Science and Technology Scholar. She earned a PhD at Duke in 2005, and after a faculty position at the Huntsman Cancer Institute at the University of Utah, she returned to Duke for the chance to forge new collaborations. "I really wanted to be exposed to new science and new ways of thinking," she said.

Oliver has made progress with small cell lung cancer by systematically profiling it. For the past 30 years, all patients with the disease have been treated the same, with chemotherapy. In the last handful of years, Oliver and other researchers have shown that they can divide the disease into at least four different subtypes, each of which responds differently to treatment. Some of this work has been translated into human clinical trials. For instance, in 2017 her lab showed that one subtype responds best to a class of drugs known as aurora kinase inhibitors, and in a clinical trial published in 2020, other researchers showed that a specific aurora kinase inhibitor worked better in patients with this subtype.

But the difference was small. "The sad part is that even though the aurora kinase inhibitor works better at extending survival in this subset of patients, the amount of benefit they get is only about two or three months," Oliver said. "That's the scale of things people see in small cell, because it's so deadly and aggressive. I believe we can do better than that."

The key to doing better, Oliver believes, is harnessing this cancer's ability to shapeshift. In a 2020 study published in CancerCell, Oliver and PhD student Abbie Ireland and colleagues reported that small cell lung cancer can cycle through different identities with ease, and that multiple subtypes are present within a single tumor.

This process is not easy to manipulate because its driven by proteins called transcription factors, which don't have a defined structure where drugs could bind. Transcription factors turn programs of genes on or off, determining a cell's reason for being, Oliver said. "Transcription factors are responsible for creating a cell's identity and its job. A transcription factor makes you a policeman versus a firefighter versus a teacher."

Oliver works to predict and then control what form the cancer will take at any given time by looking for clues in stem cell biology and early lung development. "We see that the different identities that small cell lung cancer takes on are mimicking the same identities that it had access to during embryonic development," she said. As one cell multiplies into two, then a mass of cells, then a pair of lungs, these cells take on different forms. Cancer seems to remember and make use of those identities to survive, especially in the face of good treatments.

"Certain cancer cell fates have particular needs and demands, and if you really shut down who they are, they just convert to something else," Oliver said.

This shapeshifting also happens in other cancers, including lung adenocarcinoma, which is the most common type of lung cancer that is diagnosed in people who have never smoked. "We have really good treatments for lung adenocarcinoma, and the patients have these dramatic responses. But then their tumor converts to a different fate because you've shut down the key pathway," Oliver said. "They convert to neuroendocrine tumors, which are basically smoking-associated tumors."

Oliver gravitates to the hardest problems. After her PhD at Duke and then a postdoctoral fellowship at MIT where she worked with Tyler Jacks, PhD, "the best mouse model person in the world," she started her own lab at Huntsman Cancer Institute in Utah in 2011, focusing on the neglected forms of lung cancer. "We had made a bunch of sophisticated models for lung adenocarcinoma, and lots of people were working on it," Oliver said. "But for the other lung cancer types we didn't have great models, so we couldn't ask the important questions."

Just a couple of months after Oliver arrived at Duke, she found one of those new collaborations she had been looking for, studying another neglected tumor type. Her first year at Duke was designated as protected time for moving her lab, but she agreed to help teach a grant-writing course because she saw it as a good way to meet students and learn about their research.

When Oliver read the title of the National Institutes of Health predoctoral fellowship grant application that MD-PhD candidate Jack Finlay was working on, she immediately wrote an email to him and his mentor, Bradley Goldstein, MD, PhD, associate professor of head and neck surgery and communication sciences. Finlay was using computational biology to study a rare nasal tumor called olfactory neuroblastoma. And Oliver knew of Goldstein's reputation as a leader in studying tissue and diseases inside the nose. "That really caught my attention because I knew from years ago that some of our mouse models we were using for small cell lung cancer were getting these olfactory tumors," Oliver said. "I really wanted to know what these tumors were, but I didn't know an expert in Utah in that field."

Finlay said the collaboration has given him a more nuanced understanding of the biology of the cancer that he plans to treat and study as an otolaryngologist and head and neck surgeon. "The first question we had was, are these really olfactory neuroblastomas in Dr. Oliver's mice? And we've since confirmed that they are," Finlay said. "So we think we have the first mouse model of this tumor, which is huge."

Designing a model like this from scratch would involve engineering the mouse tumors to express the same genetic mutations that are seen in human tumors, he said. Since olfactory neuroblastoma is rare and understudied, many of those details aren't known. "It's hard to even envision how you would begin to make a mouse model," he said.

Finlay is excited about the possibility of using the mice to test potential non-surgical treatments for olfactory neuroblastoma. The standard of care for these tumors is surgery, which is often extensive and disfiguring for the patient because the tumors are so aggressive. "We really don't have many options besides just taking out as much of the tissue as possible," Finlay said.

Finlay visits the Oliver lab at least once a week. "It's a fun, lively environment, whether they're having scientific discussions or troubleshooting a cell line," he said. In addition, he and Goldstein meet with Oliver, PhD student Abbie Ireland, and research technician Bryony Hawgood every couple of months for data review and presentations. "That will go on for hours," Finlay said. Pizza is usually on the table.

Early studies of the mice suggest that these olfactory tumors use some of the same means of survival as small cell lung cancer and treatment-resistant prostate cancer, Oliver said. "We hope we're going to bring together people from the prostate cancer field and the lung field and the olfactory field to appreciate that we're all studying a very similar disease."

Angela Spivey is a senior science writer and managing editor for the School of Medicines Office of Strategic Communications.

Photos by Alex Boerner. Video by Jim Rogalski.

Main image: Trudy Oliver, PhD, professor of pharmacology and cancer biology at Duke University School of Medicine and a Duke Science and Technology Scholar.

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Trudy Oliver Tracks a Deadly, Shapeshifting Tumor - Duke University School of Medicine

Fox Chase Cancer Center is Holding a ‘Be The Match’ Virtual Event – Fox Chase Cancer Center

April is National Donate Life Month, and Fox Chase Cancer Center and Temple Health are hosting a Be The Match virtual event.

PHILADELPHIA (April 6, 2023) April is National Donate Life Month, and Fox Chase Cancer Center and Temple Health are kicking off the month with a Be The Match virtual event.

Be The Match is a nonprofit organization and global leader in blood stem cell transplantsometimes called bone marrow transplantfocusing on improving outcomes, support, and resources for patients with cancers and blood diseases like sickle cell anemia. Cancers that typically affect bone marrow function include leukemias, multiple myeloma, and lymphomas, all of which originate in the blood cells. For certain types of these cancers, transplants can be an important part of treatment.

During stem cell transplantation, a patient whose stem cells have been destroyed by cancer or its treatment will receive healthy blood-forming stem cells from a donor to replace their own. These stem cells are predominately taken from blood; a small portion are taken from bone marrow. Only 30% of patients have a matching donor in their families, so the remaining 70% must search the Be The Match Registry to find a matching donor.

Fox Chases Department of Bone Marrow Transplant (BMT) and Cellular Therapies is one of the leading programs in the country. Its outpatient and inpatient units occupy the entire fifth floor of the Patient Care Center at Temple University Hospital Jeanes Campus.

To sign up for the registry, individuals between the ages of 18 and 40 can text BMT to 61474 and complete a brief health history. Be The Match will send you a cheek swab kit in the mail within a few days. From there, simply complete your swab test and return it to Be The Match using the prepaid envelope.

Using the swab kit that you send in, Be The Match determines your human leukocyte antigen (HLA) typea protein found in most cells of the bodyto compare with HLA markers of patients who need a bone marrow transplant.

It may take months or even years to find a match, and being on the registry doesnt guarantee you will ever be matched to a patient in need. A donor and recipient do not need to have the same blood type, but patients are more likely to match with donors with similar ethnic backgrounds. If you are identified as a match for a patient, Be The Match will move quickly to take the next steps in coordinating a donation as you may be the only option for a patient seeking a life-saving stem cell transplant.

There are two ways to donate blood stem cells or marrow. The first process, which is used 90% of the time, is a nonsurgical peripheral blood stem cell collection that resembles plasma donation. The second process is marrow extraction, a surgical procedure performed under anesthesia.

Many donors say they experience little to no pain during the process of donating. There can be some discomfort during recovery that varies from person to person. Side effects can include back pain, fatigue, headache, and bruising for a few days or weeks, but many donors say they would do it again to save a life.

For further information, contact Rebecca Farrell, Clinical Manager at Fox Chase, at 215-214-3738.

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Fox Chase Cancer Center is Holding a 'Be The Match' Virtual Event - Fox Chase Cancer Center

From Petri Dishes to Profits: The Lucrative World of Cell Culture Media – GlobeNewswire

Westford, USA, April 10, 2023 (GLOBE NEWSWIRE) -- The market for Cell Culture Media is projected to grow at a CAGR of 13.2% during the forecast period (2022-2030) and is expected to reach USD 14.96 billion by 2030. The market growth is fueled by a rise in demand for biopharmaceuticals, increasing investments in research and development, technological advancements, a growing awareness of cell-based therapy, and an increasing demand for personalized medicine. SkyQuest reports that the global biopharmaceutical market is expected to grow at a CAGR of 9.7% and reach USD 485 billion by 2025. Additionally, 68% of experts attribute the rising adoption of cell-based assays in drug discovery and research as a driver for the cell culture media market.

SkyQuest's latest research findings suggest that the global monoclonal antibodies market is anticipated to grow at a CAGR of 13.5% and reach USD 262.5 billion by 2027, mainly due to the increasing demand for biopharmaceuticals and the development of advanced technologies for cell culture. Finally, reports indicate that 45% of experts consider the increasing demand for biologics and biosimilars as the primary driver for the cell culture media market.

Browse in-depth TOC on "Cell Culture Media Market.

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https://www.skyquestt.com/sample-request/cell-culture-media-market

The significance of the cell culture media market lies in its provision of essential nutrients, growth factors, and other components crucial for cell growth and maintenance in diverse applications, including drug discovery, biopharmaceutical production, and tissue engineering. Rising biopharmaceutical demands and the emergence of advanced cell culture technologies spur this market's expansion.

Prominent Players in Cell Culture Media Market

Browse summary of the report and Complete Table of Contents (ToC):

https://www.skyquestt.com/report/cell-culture-media-market

Biopharmaceutical Production Segment to Drive Higher Sales due to the Rising demand for Biologics and Biosimilar, Single-use Technology, Regulatory Approvals

A recent analysis indicates that the Biopharmaceutical Production segment significantly contributed to the rapid development of the Cell Culture Media market in 2021, and this trend is expected to continue from 2022 to 2030. The demand for biologics and biosimilars, Single-use technology, and regulatory approvals drive this trend. The productivity of biopharmaceutical production has increased due to the use of advanced cell cultures technologies, such as perfusion and fed-batch processes. The Biotechnology Innovation Organization reports that over the past few decades, technological advancements have increased biopharmaceutical production's average yields by more than 100-fold. Additionally, according to SkyQuest reports, 94.7% of biopharmaceutical manufacturers are investing in advanced cell culture technologies to enhance productivity and reduce costs. The survey notes that the use of these technologies has led to a reduction in production costs by up to 30%.

According to research analysis, North America is expected to become a dominant player in the Cell Culture Media market from 2022 to 2030, with a projected growth rate of 9.82% during the forecast period, as reported by SkyQuest. The presence of many biopharmaceutical companies, well-established research infrastructure, and increasing demand for personalized medicine in the region drives this expansion. Recently, Catalent announced the expansion of its cell and gene therapy manufacturing facility in Maryland, which includes producing cell culture media and other critical raw materials, further contributing to the market growth in North America.

Reagents and Media Product Segment to Exhibit Strong Growth Due to Demand for Lightweight and Advanced Wheels and Brakes Systems

The Reagents and Media Product segment has emerged as the dominant method in the Cell Culture Media market in 2021 and is expected to retain its lead from 2022 to 2030, driven by the increasing demand for biologics and biosimilars, the growth of the biopharmaceutical industry, and the development of advanced cell culture technologies. SkyQuest reports that the reagents and media product segment also benefits from the growing demand for automation and high-throughput screening in drug discovery. The global high-throughput screening market is expected to grow at a CAGR of 7.8% during the forecast period due to the increasing demand for automated systems and the development of novel screening technologies.

The Asia Pacific region has emerged as a significant force in the Cell Culture Media market and is expected to retain its leading position by 2030, as forecasted by SkyQuest, with a projected CAGR of 12.97% during the forecast period. This expansion can be attributed to the growing number of pharmaceutical companies and increasing investment in regional research and development.

A comprehensive analysis of the major players in the Cell Culture Media market has been recently conducted in a report. The report encompasses various aspects, including collaborations, mergers, innovative business policies, and strategies, providing valuable insights into key trends and breakthroughs in the market. Furthermore, the report scrutinizes the market share of the top segments and presents a detailed geographic analysis. Lastly, the report highlights the major players in the industry and their endeavors to develop innovative solutions to cater to the growing demand.

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Key Developments in Cell Culture Media Market

Key Questions Answered in Cell Culture Media Market Report

Related Reports in SkyQuests Library:

Global Research Antibodies and Reagents Market

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From Petri Dishes to Profits: The Lucrative World of Cell Culture Media - GlobeNewswire

Century Therapeutics Announces Leadership Changes – GlobeNewswire

Lalo Flores, Ph.D., steps down as Chief Executive Officer and member of Board of Directors; Greg Russotti, Ph.D., Chief Technology Officer, assumes role of ad-interim Chief Executive Officer

Michael C. Diem, M.D., promoted to Chief Financial Officer

Hy Levitsky, M.D., rejoins as President of Research and Development

PHILADELPHIA, April 12, 2023 (GLOBE NEWSWIRE) -- Century Therapeutics (NASDAQ: IPSC), an innovative biotechnology company developing induced pluripotent stem cell (iPSC)-derived cell therapies in immuno-oncology, today announced the appointment of Greg Russotti, Ph.D., as ad-interim Chief Executive Officer, effective April 11, 2023. Dr. Russotti, who has served as the Companys Chief Technology Officer since January 2020, is succeeding Lalo Flores, Ph.D., who has stepped down as Chief Executive Officer and as a member of the Companys Board of Directors to pursue other opportunities. In addition, effective April 11, 2023, Michael C. Diem, M.D., was promoted to the role of Chief Financial Officer, and Hy Levitsky, M.D., assumed his prior role as President of Research and Development.

The Board of Directors has commenced a search to identify a permanent Chief Executive Officer.

Lalo has played a key role in advancing Century, a premier cell therapy company, to where it is today. On behalf of the entire Board of Directors, we wish Lalo success and thank him for his service, said Joe Jimenez, Chairman of the Board. Greg is a true leader in the cell therapy space who we believe can build upon the Companys strong foundation with his significant clinical and commercial expertise. As Century enters an exciting new stage of growth, we look forward to continuing to leverage his extensive experience.

Mr. Jimenez added, Additionally, I would like to congratulate Mike Diem on his promotion to Chief Financial Officer, and I am pleased to welcome Hy Levitsky back to Century. Both Mike and Hy have been instrumental in Centurys success to date, and we look forward to their continued contributions as the Company advances its next generation platform and robust portfolio of cell therapy product candidates.

Greg Russotti, Ph.D., ad-interim Chief Executive Officer

Prior to joining Century, Dr. Russotti served as Vice President of Cell Therapy Development and Operations at Celgene. While at Celgene, he guided chemistry, manufacturing and controls efforts for five different cell therapy products to clinical-stage development. Dr. Russotti was also a leader in establishing in-house clinical manufacturing at Celgene, and in building Celgenes first commercial CAR T manufacturing facility. Prior to Celgene, he held various leadership roles at Merck Research Laboratories, developing vaccines and monoclonal antibodies for clinical and commercial manufacturing. He received his B.S. and M.S. degrees in Chemical Engineering from Rensselaer Polytechnic Institute, and his Ph.D. in Chemical and Biochemical Engineering from Rutgers University. Dr. Russotti has held a visiting professorship in Rutgers Biomedical Engineering department since 2008. He also serves as Industrial Executive Board Member of the Marcus Center for the Commercialization of Cell Therapies at Georgia Tech, and as an Executive Committee member of the National Science Foundation-funded Center for the Manufacturing of Advanced Therapeutics at Georgia Tech.

I am honored to assume this role, and I look forward to building upon our accomplishments to date to execute on our vision of delivering transformative allogeneic cell therapies to patients, said Dr Russotti. With a solid balance sheet, which we expect to fund operations into 2026, we believe we are well-positioned to continue to deliver on our key platform and program milestones.

Michael C. Diem, M.D., Chief Financial Officer

Dr. Diem, who joined Century in 2020, most recently served as the Companys Chief Business Officer. Prior to joining Century, he was Senior Vice President of Business and Corporate Development at Amicus Therapeutics, and prior to that, he held a similar role at Aevi Genomic Medicine. Earlier in his career, Dr. Diem was the Global Head of Corporate Strategy and Corporate Development at AstraZeneca, where he was responsible for mergers and acquisitions, divestitures, and managed the companys strategic investment activities and MedImmune Ventures. At GlaxoSmithKline (GSK), he led business development for the Companys rare disease business unit, and was also a partner in GSKs corporate venture firm, SR One, Limited. Dr. Diem obtained his M.D. from the Rutgers-Robert Wood Johnson Medical School, and an M.B.A. from Case Western Reserve University. He completed his medical training at Duke University and is a Kauffman Fellow.

Hy Levitsky, M.D., President of Research and Development

Dr. Levitsky previously served as Centurys President, Research and Development from 2019 until early 2023. Prior to joining the Company, he served as Executive Vice President and Chief Scientific Officer at Juno Therapeutics, Inc., and was also Head of Cancer Immunotherapy Experimental Medicine at F. Hoffmann-La Roche & Co. Previously, Dr. Levitsky was Professor of Oncology, Medicine, and Urology at The Johns Hopkins University School of Medicine and the Sidney Kimmel Comprehensive Cancer Center, and the Scientific Director of the George Santos Bone Marrow Transplant Program at The Johns Hopkins University. He currently serves as a member of the Board of Directors of Replimune, Prokarium, and Carisma Therapeutics. Dr. Levitsky obtained his M.D. from The Johns Hopkins University School of Medicine.

About Century Therapeutics

Century Therapeutics (NASDAQ: IPSC) is harnessing the power of adult stem cells to develop curative cell therapy products for cancer that we believe will allow us to overcome the limitations of first-generation cell therapies. Our genetically engineered, iPSC-derived iNK and iT cell product candidates are designed to specifically target hematologic and solid tumor cancers. We are leveraging our expertise in cellular reprogramming, genetic engineering, and manufacturing to develop therapies with the potential to overcome many of the challenges inherent to cell therapy and provide a significant advantage over existing cell therapy technologies. We believe our commitment to developing off-the-shelf cell therapies will expand patient access and provide an unparalleled opportunity to advance the course of cancer care. For more information on Century Therapeutics please visit http://www.centurytx.com.

Century Therapeutics Forward-Looking Statement

This press release contains forward-looking statements within the meaning of, and made pursuant to the safe harbor provisions of, The Private Securities Litigation Reform Act of 1995. All statements contained in this press release, other than statements of historical facts or statements that relate to present facts or current conditions, including but not limited to, statements regarding our clinical development plans and timelines, are forward-looking statements. These statements involve known and unknown risks, uncertainties and other important factors that may cause our actual results, performance, or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements. In some cases, you can identify forward-looking statements by terms such as may, might, will, should, expect, plan, aim, seek, anticipate, could, intend, target, project, contemplate, believe, estimate, predict, forecast, potential or continue or the negative of these terms or other similar expressions. The forward-looking statements in this press release are only predictions. We have based these forward-looking statements largely on our current expectations and projections about future events and financial trends that we believe may affect our business, financial condition, and results of operations. These forward-looking statements speak only as of the date of this press release and are subject to a number of risks, uncertainties and assumptions, some of which cannot be predicted or quantified and some of which are beyond our control, including, among others: our ability to successfully advance our current and future product candidates through development activities, preclinical studies, and clinical trials; our ability to obtain FDA acceptance for our future IND submissions and commence clinical trials on expected timelines, or at all; our reliance on the maintenance of certain key collaborative relationships for the manufacturing and development of our product candidates; the timing, scope and likelihood of regulatory filings and approvals, including final regulatory approval of our product candidates; the impact of the COVID-19 pandemic, geopolitical issues and inflation on our business and operations, supply chain and labor force; the performance of third parties in connection with the development of our product candidates, including third parties conducting our future clinical trials as well as third-party suppliers and manufacturers; our ability to successfully commercialize our product candidates and develop sales and marketing capabilities, if our product candidates are approved; and our ability to maintain and successfully enforce adequate intellectual property protection. These and other risks and uncertainties are described more fully in the Risk Factors section of our most recent filings with the Securities and Exchange Commission and available at http://www.sec.gov. You should not rely on these forward-looking statements as predictions of future events. The events and circumstances reflected in our forward-looking statements may not be achieved or occur, and actual results could differ materially from those projected in the forward-looking statements. Moreover, we operate in a dynamic industry and economy. New risk factors and uncertainties may emerge from time to time, and it is not possible for management to predict all risk factors and uncertainties that we may face. Except as required by applicable law, we do not plan to publicly update or revise any forward-looking statements contained herein, whether as a result of any new information, future events, changed circumstances or otherwise.

For More Information: Company: Elizabeth Krutoholow investor.relations@centurytx.comInvestors and Media: Melissa Forst/Maghan Meyers century@argotpartners.com

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Century Therapeutics Announces Leadership Changes - GlobeNewswire

Living at high altitude leads to longer life by changing metabolism – Earth.com

An estimated two million people worldwide reside above 4,500 meters (14,764 feet) in elevation, comparable to the heights of Mount Rainier, Mount Whitney, and numerous peaks in Colorado and Alaska. Intriguingly, these individuals have been observed to have lower rates of metabolic diseases, such as diabetes, coronary artery disease, hypercholesterolemia, and obesity. Researchers supported by the U.S. National Science Foundation at Gladstone Institutes have recently made strides in understanding this phenomenon.

The scientists discovered that chronic exposure to low oxygen levels, as experienced at high altitudes, altered the way mice metabolized sugars and fats. The study, published in the journal Cell Metabolism, offers insights into the metabolic differences in people living at high altitudes and suggests potential new treatments for metabolic diseases.

When an organism is exposed to chronically low levels of oxygen, different organs reshuffle their fuel sources and their energy-producing pathways, explained Isha Jain, senior author of the study. We hope these findings will help us identify metabolic switches that might be beneficial for metabolism even outside of low-oxygen environments.

At sea level, where a third of the global population resides, oxygen accounts for approximately 21% of the air we breathe. However, at elevations above 4,500 meters, oxygen makes up a mere 11% of the air. Despite these lower oxygen levels, known as hypoxia, people can adapt and thrive in these conditions.

Previous research on hypoxias impact has often been limited to isolated cells or cancerous tumors, which are commonly oxygen-deficient. Jains group aimed to investigate the long-term effects of hypoxia on organs throughout the body. They collaborated with colleagues at Gladstone and the University of California, San Francisco, to house adult mice in pressure chambers containing 21%, 11%, or 8% oxygen levels all of which are survivable by humans and mice.

Over three weeks, the researchers monitored the mices behavior, temperature, carbon dioxide levels, blood glucose levels, and used positron emission tomography (PET) scans to study nutrient consumption by different organs. In the initial days of hypoxia, mice in 11% or 8% oxygen environments exhibited reduced mobility and periods of complete stillness.

However, by the end of the third week, their movement patterns normalized. Likewise, their blood carbon dioxide levels, which typically decrease when mice or humans breathe faster to compensate for low oxygen, initially dropped but returned to normal levels by the end of the study.

The animals metabolism, on the other hand, appeared to be more permanently affected by hypoxia. Mice in hypoxic cages experienced decreases in blood glucose levels and body weight, with neither returning to pre-hypoxic levels.

These metabolic changes parallel those observed in humans living at high altitudes and are associated with a reduced risk of diseases, including cardiovascular disease. This understanding of hypoxias contribution could pave the way for developing new drugs that replicate these beneficial effects, offering hope for those suffering from metabolic diseases.

There is a growing body of research focused on understanding the biological processes of aging and developing strategies to extend human lifespan. Some of the prominent areas of research include:

These research areas, along with many others, represent the ongoing efforts to unravel the complex biology of aging and develop interventions that can promote healthy aging and extend human lifespan.

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Living at high altitude leads to longer life by changing metabolism - Earth.com

Sana Biotechnology (SANA) Announces Publication of Preclinical … – StreetInsider.com

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Sana Biotechnology, Inc. (NASDAQ: SANA), a company focused on changing the possible for patients through engineered cells, today announced that Science Translational Medicine has published a paper titled Human hypoimmune primary pancreatic islets avoid rejection and autoimmunity and alleviate diabetes in allogeneic humanized mice. The paper details data from a series of ten in vivo experiments demonstrating the insulin-normalization activity, persistence, immune evasion, and lack of immunogenicity of human hypoimmune-modified islet cells, which cluster into effective endocrine organoids termed pseudo islets.

The replacement of defective or missing cells has been the goal for many diseases; however, immune rejection results in either systemic immunosuppression or therapeutic failure. Sanas proprietary hypoimmune platform was developed to solve this problem, said Steve Harr, Sanas President and CEO. The Science Translational Medicine paper details data demonstrating that hypoimmune pseudo islets developed with our hypoimmune technology survived and were able to reverse diabetes without any immunosuppression in humanized mice. Eliminating the need for insulin administration and reversing diabetes with normalization of blood glucose levels, and doing this without immunosuppression, would be a transformational advance for patients. Insights from this research along with an expected investigator-sponsored trial this year will inform the development plan for our SC451 product candidate in type 1 diabetes as we move forward with our goal of submitting an IND in 2024.

HIP Pancreatic Islet Cells Survive, Persist, and Escape Allogeneic RejectionSana generated human hypoimmune (HIP) pseudo islets (p-islets) and wild-type (wt) p-islets that were similar in size, cell type composition, and in vitro insulin secretion. The survival of the p-islets and their cell composition was assessed in immunocompetent, diabetic allogeneic humanized NSG-SGM3 mice. HIP or wt p-islet clusters were injected into the hindlimb muscle and were recovered on the same day or 7 or 28 days later. Wt p-islets could only be recovered on the same day and were fully rejected and dissolved at later time points. By contrast, the total cell count and cell composition of HIP islets did not change over time.

In another experiment, analyses were conducted a month following exposure to HIP and wt p-islets. There were no traces of wt p-islet grafts found in any animals after one month. Recovered splenocytes and serum from the wt p-islet treated animals showed markedly activated T cells (analyzed by ELISPOT) and donor-specific antibodies (analyzed by flow cytometry) against the grafts in the wt p-islet group, demonstrating a strong adaptive allogeneic immune response. By contrast, HIP p-islets showed the same morphology as before transplantation and contained alpha, beta, and delta cells. No immune cell infiltrate was observed in or around the HIP p-islet cells. Additionally, no adaptive allogeneic immune response was observed in humanized mice that received HIP p-islets and diabetes in these mice was alleviated. Confirmatory killing assays showed killing of wt p-islets and no killing of HIP p-islets.

HIP Islet Cells Control Insulin Similarly to Unedited Wild-Type Islet Cells in Immunodeficient MiceThe ability to control diabetes was assessed in immunodeficient NSG mice to remove the variable of immune rejection of allogeneic cells, enabling the comparison of wt and HIP p-islets. Diabetes was induced using streptozotocin (STZ) and all mice had fasting glucose concentrations >400 mg/dl on the day of p-islet graft transplantation. Wt and HIP p-islets both achieved glycemic control within approximately 2 weeks and generated similar c-peptide concentrations one months after transplantation. These functional data confirmed that HIP p-islet cells maintained endocrine function comparable to wt p-islets and showed unimpaired resilience toward the transplantation procedure.

HIP Islet Cells Ameliorate Diabetes in Models of Autoimmunity: NOD Mice as well as Humanized Autoimmune Mice The ability of HIP islet cells to avoid autoimmunity was assessed in two different models. The first set of experiments were in the NOD mouse, which is the primary animal model for studying autoimmunity in diabetes due to the similarities to the human disease. These studies demonstrate that mouse HIP p-islets survive while syngeneic p-islets are rejected due to autoimmune killing. Additionally, the impact of autoimmunity was studied in a humanized, diabetic autoimmune mouse. To generate a humanized, autoimmune mouse, immune cells and iPSCs were generated from PBMCs collected from a person with type 1 diabetes (T1D). Mice were engrafted with the T1D immune cells and diabetes was induced. The iPSCs were then either hypoimmune-modified or mock-modified, differentiated into islet cells, and transplanted into these immunocompetent, diabetic humanized mice to study autoimmunity in vivo. All HIP iPSC-derived p-islets survived and glycemic control was achieved in all recipients of HIP iPSC-derived p-islets. In contrast, all autologous, mock-modified iPSC-derived p-islets were fully rejected within 10 days due to autoimmunity and showed no effect on blood glucose, even temporarily, and animals had no detectable c-peptide after one month.

About Sanas Hypoimmune PlatformSanas hypoimmune platform is designed to create cells ex vivo that can hide from the patients immune system to enable the transplant of allogeneic cells without the need for immunosuppression. We are applying hypoimmune technology to both donor-derived allogeneic T cells, with the goal of making potent and persistent CAR T cells at scale, and pluripotent stem cells, which can then be differentiated into multiple cell types at scale. Preclinical data from a variety of cell types demonstrate that these transplanted allogeneic cells can evade both the innate and adaptive arms of the immune system while retaining their function. Our most advanced programs using hypoimmune technology include our allogeneic CAR T program targeting CD19+ cancers, our allogeneic CAR T program targeting CD22+ cancers, our allogeneic CAR T program targeting BCMA+ cancers, and our stem-cell derived pancreatic islet cell program for patients with type 1 diabetes.

About Sana BiotechnologySana Biotechnology, Inc. is focused on creating and delivering engineered cells as medicines for patients. We share a vision of repairing and controlling genes, replacing missing or damaged cells, and making our therapies broadly available to patients. We are a passionate group of people working together to create an enduring company that changes how the world treats disease. Sana has operations in Seattle, Cambridge, South San Francisco, and Rochester. For more information about Sana Biotechnology, please visit https://sana.com/.

Cautionary Note Regarding Forward-Looking StatementsThis press release contains forward-looking statements about Sana Biotechnology, Inc. (the Company, we, us, or our) within the meaning of the federal securities laws, including those related to the companys vision, progress, and business plans; expectations for its development programs, product candidates, and technology platforms, including its pre-clinical, clinical, and regulatory development plans and timing expectations, including the expected timing of IND submissions for the Companys product candidates and indications for which the Company is developing its product candidates and for which such INDs will be submitted, and expected impact of data from pre-clinical studies of cells made using hypoimmune technology and from an investigator-sponsored trial using hypoimmune primary human islet cells in patients with type 1 diabetes (the IST), including the potential of pre-clinical data and the IST to provide insight that will inform development of its SC451 product candidate; expectations regarding the IST, including the ability to initiate the IST and expected timing, substance, and availability of data therefrom; the potential ability of the hypoimmune platform to create cells ex vivo that can hide from the patients immune system to enable the transplant of allogeneic cells without the need for immunosuppression, and the potential benefits associated therewith; and the potential ability to make potent and persistent CAR T cells at scale and of hypoimmune pluripotent stem cells to differentiate into multiple cell types at scale. All statements other than statements of historical facts contained in this press release, including, among others, statements regarding the Companys strategy, expectations, cash runway and future financial condition, future operations, and prospects, are forward-looking statements. In some cases, you can identify forward-looking statements by terminology such as aim, anticipate, assume, believe, contemplate, continue, could, design, due, estimate, expect, goal, intend, may, objective, plan, positioned, potential, predict, seek, should, target, will, would and other similar expressions that are predictions of or indicate future events and future trends, or the negative of these terms or other comparable terminology. The Company has based these forward-looking statements largely on its current expectations, estimates, forecasts and projections about future events and financial trends that it believes may affect its financial condition, results of operations, business strategy and financial needs. In light of the significant uncertainties in these forward-looking statements, you should not rely upon forward-looking statements as predictions of future events. These statements are subject to risks and uncertainties that could cause the actual results to vary materially, including, among others, the risks inherent in drug development such as those associated with the initiation, cost, timing, progress and results of the Companys current and future research and development programs, preclinical and clinical trials, as well as the economic, market and social disruptions due to the ongoing COVID-19 public health crisis. For a detailed discussion of the risk factors that could affect the Companys actual results, please refer to the risk factors identified in the Companys Securities and Exchange Commission (SEC) reports, including but not limited to its Annual Report on Form 10-K dated March 16, 2023. Except as required by law, the Company undertakes no obligation to update publicly any forward-looking statements for any reason.

Investor Relations & Media:Nicole Keith[emailprotected][emailprotected]

Source: Sana Biotechnology, Inc

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Sana Biotechnology (SANA) Announces Publication of Preclinical ... - StreetInsider.com

The Explorers: A Passion for Science Leads to New Territory – University of California San Diego

Unusual Breadth

This quest soon led them to seek out real-world problems that could have a bigger impact on peoples lives than basic science. They moved to the West Coast, where they pursued a mix of research and development jobs in biotechincluding at Amgen and Invitrogen (acquired by Thermo Fisher)and at universities including UC Berkeley (Molokanova), UC San Diego and Stanford University (Savtchenko).

These experiences working at intersection of physics and biology coupled with decades of work across multiple scenarios in academics and industry gave the couple a unique perspective on many of the biggest problems in neuroscience and drug discovery, as well as the business processes that helped or hindered progress.

So, as they discussed whether to start their own companies, they didnt have to deliberate for long.

It was pretty clear to me that the science was coming along nicely, and that our contribution [as entrepreneurs] would be serious, meaningful, said Savtchenko.

One major challenge the pair had observed in the biotech industry involved initial testing of potential drug compoundsresults that informed whether compounds would be pursued or discarded from consideration for further development as medicines.

Savtchenko noted that biotech and pharmaceutical companies spend billions of dollars on screening drug compounds for safety and activityin vitro(in cell culture), yet the environment in plastic cell culture dishes drastically differs from the human body, especially for nerve cells (a.k.a. neurons) and heart cells (a.k.a. cardiomyocytes).

The biggest difference between neurons in the brain and neurons in a cell culture dish is whether they receive external input or not, Savtchenko explained. From the very first moment of our existence, it is normal and, in fact, necessary for our brains to be constantly bombarded by various signals (e.g., stimuli from sight, hearing, feeling, tasting)the results determine our development, define our individual personalities and, often, affect our health.

He continued, To discover drugs that can fix aberrations in brain activity and heal a patient, it is imperative to test the drug effects on functionally active, input-receiving, dynamic response-producing neurons. Otherwise, clinical studies in human patients might produce drastically different outcomes than priorin vitrostudiesresulting in failed projects, loss of multibillion dollar investments, and disappointment for millions of patients.

The development of medication that could affect the heart faces similar challenges. Testing for drug cardiotoxicity is often performed in highly artificial conditionsin an electrically insulated culture dish of human stem-cell derived cardiomyocytes, spontaneously contracting at a single frequency. In real-life, adult heart rates can vary almost two-fold over the course of a day in response to changing conditions.

Highlighting the importance of such testing, in recent decades several blockbuster drugs have been removed from the market because they were linked to irregular heartbeat, accounting for 30% of all post-approval withdrawals.

Savtchenko and Molokanova wanted to find a way to safely and reliably stimulate cells in a dish while testing their response in the presence of drug compounds so that the results of these screening studies would better predict the drugs affect in humans. Reaching this goal would mean that fewer drugs would fail at the last stages of drug discovery process, resulting in safer, more efficient, and less expensive drugs.

After her industry experience working with different materials, including semiconductor quantum dots, to stimulate cells in culture, Molokanova hit on the idea to harness the unique properties of a new two-dimensional carbon allotrope, graphene.

Graphene had been discovered by Andre GeimandKonstantin Novoselov (coincidentally fellow alumni of Savtchenkos alma mater, MIPT), who were awarded the 2010 Nobel Prize in Physics for this finding. In the Nobel announcement, the Royal Swedish Academy of Sciencesdescribedgraphene as a thin flake of ordinary carbon, just one atom thick [with] exceptional properties that originate from the remarkable world of quantum physics.

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The Explorers: A Passion for Science Leads to New Territory - University of California San Diego