Daily Archives: February 9, 2022

In biopharma, we often frame our genetics as a Goliathan adversary that must be compromised with or circumvented rather than overcome. We focus on using our genes the same way our body does: as a source of information concerning how our system operates and as a means of identifying and predicting the potential one has to develop certain conditions or diseases.

Our genes arent just a source of information, though; theyre also a source of creative inspiration and ingenious solutions for predestined problems. Instead of looking to our genes for a culprit that we can subject to interrogatory treatments, we could also look at our genes as a potential source from which to derive therapeutics.

Old Order Amish Variant Protects Against Heart Disease

In early December 2021, the University of Marylands School of Medicine (UMSOM) announced the discovery of a recently uncovered genetic variation linked to lower levels of fibrinogen and LDL cholesterol, suggesting that this may be behind the significantly lower risk of heart disease exhibited by those who express it.

While its unclear how exactly this mutation is influencing the amount of LDL cholesterol and fibrinogen in a given patients bloodstream, a general population study of over 500,000 individuals showed that anyone carrying a unique version of the B4GALT1 gene was 35% less likely to develop cardiovascular diseases.

However, this particular genetic variant is only present in less than a hundred people for about every million. Its highest prevalence by population size anywhere in the United States by far is found within the Old Order Amish community of Lancaster, Pennsylvania, where about 12% of the population possesses the B4GALT1 variation.

Through their longstanding partnership with members of the Amish community and collaboration with the Regeneron Genetics Center (RGC), the University of Marylands School of Medicine has collected and sequenced almost 7,000 samples from Amish research participants dating back to 1995.

This allowed them to pinpoint the exact variant and replicate its expression in mice. The mouse model, encoding for this gene mutation, also showed decreased levels of LDL cholesterol and fibrinogen, confirming the effect of this variant, said Giusy Della Gatta, Ph.D. RGC senior staff scientist and study senior co-author This model represents an invaluable tool to unravel the molecular mechanisms that help protect against cardiovascular disease.

This marks the first time that a genetic variant with the potential to decrease a patients risk for heart disease has been uncovered. While links between genetic mutations and increased risk have already been established, this discovery opens a new door into preventative cardiovascular care possibilities that may produce novel therapeutic drugs.

The genetic variant appears to either control the synthesis of cholesterol and fibrinogen or accelerate their clearance from the blood, which protects the heart. This finding could lead to targeted drugs that mimic the action of this variant to keep arteries free of plaque and clots, said study leader May Montasser, Ph.D., a member of UMSOMs program for personalized and genomic medicine and assistant professor of medicine.

It will be a long time, if ever, before this research produces an in-hand pharmaceutical product; but the newfound knowledge that there could be more variants with similar pharmacologic potential means it will only be a matter of time before one makes a real difference.

CCR5-32 Mutation Repurposed for COVID-19 Treatment

Originally discovered and described in the mid-1990s, the CCR5-32 mutation made waves for the resistance to HIV infection and AIDS development it apparently bestowed upon its host. Although it isnt exceptionally common, this mutation is present in about 10% of the population on average from Europe to western Asia.

Just a single copy of this mutation would protect a person against HIV infection, and slow the progression of the disease to AIDS if they did contract it, while a second copy would make a person almost completely immune to infection. However, this mutation only endows resistance in the case of HIV-1, and not for any other HIV variants.

Thats because the CCR5-32 mutation only disrupts the function of a singular variety of immune cell receptor, one that HIV-1 happens to be dependent on in order to infect the macrophage cells of their host. The less common strains of HIV are less dependent on the CCR5 receptor, making this mutation less effective at conferring resistance.

Now, creative minds at the late-stage biotechnology company CytoDyn, Inc. are crafting new tricks out of old hat research, announcing in late December that the U.S. Food and Drug Administration had given it the affirmative to commence with a Phase III trial to evaluate the efficacy and safety of CCR5 receptor antagonist leronlimab against COVID-19 in the critically ill population.

As it turns out, the same advantage against HIV-1 possessed by a person with the inactive CCR5 variant potentially doubles as resistance to any virus that capitalizes on or manipulates that receptor an umbrella that might include COVID-19. By artificially deactivating the CCR5 receptors, leronlimab also appears to encourage a stronger and more balanced immune response in patients critically afflicted with COVID-19.

The submission of the trials protocol was announced less than two weeks prior to the aforementioned press release and outlines a four-week treatment period, so its safe to say that it might be another month or two before the results are finalized and the analysis is made available for the public.

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The Unique Therapeutic Possibilities Posed by Rare Human Genes - BioSpace

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How are physicians and scientists including underrepresented groups in the promise of precision medicine? Baylor College of Medicine will host a panel of experts to discuss this topic and the intersection of identity and genetics at an upcoming Evenings with Genetics virtual seminar on Tuesday, Feb. 15, at 7 p.m.

The webinar, titled Race and Genetics: Perspectives on Precision Medicine, will discuss the complexity of racial identity and its impact on health and disease. Panelists will address specific examples of factors affecting diseases in genetically and culturally diverse populations and the foundations needed to deliver equitable precision medicine to communities of color.

The evenings panelists are Vence L. Bonham, Jr., acting deputy director of the National Human Genome Research Institute (NHGRI) and associate investigator of the NHGRI social and behavioral research branch, and Dr. Fatimah Jackson, professor of biology and former director of the Cobb Research Laboratory at Howard University. Dr. Cherilynn Shadding will join the panel as a guest parent speaker.

Evenings with Genetics is a regular speaker series hosted by Baylor and Texas Childrens Hospital that offers the most current information on care and research advances for many genetic conditions. This event is co-sponsored by the Baylor Office of Diversity, Equity and Inclusion.The program is free and open to the public, but registration is required. A Zoom link will be sent to all registered participants the day before the seminar. For more information, call 713-798-3148 or visit the event registration page.

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Evenings with Genetics: race and precision medicine - Baylor College of Medicine News

ORIGINA Genetic History of the AmericasBy Jennifer Raff

Its Anthropology 101. At the end of the last ice age, around 13,000 years ago, retreating glaciers created an inland corridor connecting Siberia to the Americas. People from northeast Asia crossed the Bering Strait land bridge and entered a new world. From there, these people often given the name Clovis, after a New Mexico site that was rich with the distinctive stone tools they made rapidly spread and successfully adapted to the various ecologies they encountered. All Native Americans can trace their ancestry back to these First Peoples.

But, according to the University of Kansas anthropological geneticist Jennifer Raff, thats not quite how it happened.

In her new book, Origin: A Genetic History of the Americas, Raff beautifully integrates new data from different sciences (archaeology, genetics, linguistics) and different ways of knowing, including Indigenous oral traditions, in a masterly retelling of the story of how, and when, people reached the Americas. While admittedly not an archaeologist herself, Raff skillfully reveals how well-dated archaeological sites, including recently announced 22,000-year-old human footprints from White Sands, N.M., are at odds with the Clovis first hypothesis. She builds a persuasive case with both archaeological and genetic evidence that the path to the Americas was coastal (the Kelp Highway hypothesis) rather than inland, and that Beringia was not a bridge but a homeland twice the size of Texas inhabited for millenniums by the ancestors of the First Peoples of the Americas.

Throughout, Raff effectively models how science is done, how hypotheses are tested, and how new data are used to refute old ideas and generate new ones.

As a paleoanthropologist who works on fossils of ancient human ancestors living millions of years ago, Ive never fully grasped why my colleagues who study the peopling of the Americas so fervently argue over a few thousand years. But Raff helps the reader understand why those several thousand years matter in terms of identifying source populations for the First Peoples of the Americas, the route they took (coastal versus inland) and the ecological challenges they faced. An informed and enthusiastic guide throughout, Raff takes the reader from underground caverns in Belize to a clean lab at the University of Kansas where ancient DNA is tediously teased from old bones. She explains difficult to understand concepts geoarchaeology, coalescence times, biodistance with well-placed sidebars. The book is richly referenced, and informative footnotes and endnotes give readers an opportunity to take a deeper dive if they wish.

Our job as anthropologists is to breathe life into the past, to retell the stories of our ancestors and extinct relatives. We do not work with lifeless old bones or inert molecules but with the precious, fragmentary remains of once living, breathing, thinking individuals who laughed, cried, lived and died.

As Raff explains, We have promised to treat the small scraps of bone and teeth with respect and mindfulness that they are cherished ancestors, not specimens. Sprinkled through Origin are lovely vignettes of life thousands of years ago. Raff playfully imagines how the Yana River boys lost their deciduous teeth in a Siberian river 31,000 years ago. She poignantly fills a page with the sorrow a family must have felt as they placed the limp body of their 2-year-old boy into the earth in south-central Nevada 12,600 years ago. Through a combination of rigorous science and a universal humanity, Raff gives ancient people a voice.

The first few chapters of Origin detail the long history of archaeology in the Americas. Here, we meet the usual characters Thomas Jefferson, Ales Hrdlicka, Franz Boas but also folks who were new to me. People like Jos de Acosta, a Jesuit priest who long ago predicted that the Indigenous peoples of the Americas were related to northeast Asian populations. And George McJunkin, a formerly enslaved man who made one of the most important archaeological discoveries of the 20th century at Folsom, N.M.

Throughout Origin, Raff takes on pseudoscientific nonsense rooted in bigotry and colonial thinking. She eviscerates claims of lost civilizations founded on the racist assumption that Indigenous people werent sophisticated enough to construct large, animal-shaped or pyramidal mounds and therefore couldnt have been the first people on the continent. She convincingly disposes of the Solutrean hypothesis of ancient Europeans in the Americas with logic and evidence. It puzzles her (and me) that people interested in this topic watch ill-informed documentaries on the History Channel when the true histories, evident in genetics, oral traditions and archaeology, are exciting enough.

Given the fast and furious pace of discovery in this field, Raff is clear that not everyone will agree with her interpretations of the data. All scientists must hold themselves open to the possibility that we could be wrong, and it may very well be that in five, 10 or 20 years, this book will be as out of date as any other, she writes. That possibility is what makes working in this field so rewarding. That, she explains, is how science is done.

While science is the most objective way of understanding the natural world that humans have ever devised, it is still done by an emotional, subjective primate us. Raff celebrates science, but also calls attention to the many ways science has harmed Indigenous communities. Origin details mistrust between some Native communities and helicopter scientists who have swooped into their lands and exploited them for their DNA without inviting input and participation from all stakeholders. The hashtag #decolonizescience looks good on Twitter and the concept sounds good in grants, but it rings hollow unless it is put into practice. Raff provides a road map for how to do this and convincingly argues why this must be the future of our science. In fact, Origin opens with the discovery of 10,000-year-old human bones from Shuk Ka Cave, Alaska, and details the constructive partnerships, built on transparency and trust, that emerged between scientists, Indigenous communities and federal agencies.

My only quibble with this outstanding book is that we dont learn who Raff herself is and how she personally has contributed to this work through her scholarship until halfway through Origin. At the end of the book, she describes herself as one obscure researcher from a small lab. To be sure, there are much bigger labs than hers, but I think shes being too modest. Jennifer Raff is a well-published scholar and accomplished scientific communicator who has contributed important insights into the genetic history and movement patterns of Indigenous Americans. She is at the forefront of a culture change in our science. And now she has written the book anyone interested in the peopling of the Americas must read.

Originally posted here:
Did the First Americans Arrive via Land Bridge? This Geneticist Says No. - The New York Times

Scientists identified an odor receptor that detects a synthetic musk used in fragrances, and another that detects underarm odor. Maskot via Getty Images

Humans may be slowly losing their sense of smell, according to new study published in PLoS Genetics last week..

When scientists tested individuals' perceptions of various smells,they found evidence thathumans' sense of smell is declining over evolutionary time. The team also discovered two new receptors in the nose that help distinguish between certain pleasant andrepulsiveodors.

When odor molecules in the air stimulate specialized nerve cells that line the nose, the brain interprets it as a scent, or combination of scents. Humans have around 800 olfactory receptor genes that can have minor variations, which change how an odor is perceived. The new resultshelpexplain why the fragranceof a specific perfume, for example, may seem pleasant to some and overpowering to others.

Were still, I would say, surprisingly ignorant about what all the olfactory receptors do and how they interact with each other to encode olfactory percepts, says Joel Mainland, a neuroscientist at Monell Chemical Senses Center and author of the research, to the Guardians Nicola Davis.

In a collaborative study between scientists in the United States and China,the team first looked at thegenesof 1,000 Han Chinese people to see howgeneticsplayed a role in scent perception. They exposed the study participants to ten common odors and asked them how they perceived each smell. The researcher then repeated the experiment for six odors in an ethnically diverse population of 364 participants. Eachperson rated the intensity and pleasantness of a given odor on a 100-point scale, which the scientists then compared their genome.

The study revealedtwo new receptors: one that detects a synthetic musk used in fragrances, and another that detects underarm odor. Because each participant had different versions of the musk and underarm odor receptor genes, those genetic variations affected how the person perceived the scents. Almost a quarter of participants couldnt smell the musk scent, for example, Catherine Schuster-Bruce reports for Business Insider.

Its really rare to find an effect thats as large as what we saw for this one receptor on the perception of the musk odor, says study author Marissa Kamarck, a neuroscientist at the University of Pennsylvania, to Sam Jones for the New York Times.

Kamarck and her colleagues say their results support the controversial hypothesis that primates smelling ability has slowly declined over time due to genetic changes. When the team looked at their results in combination with previously published studies on genes and scent, they found that participants with the ancestral versions of the scent receptorsthose shared with non-human primatestended to rate the corresponding odor as more intense.

While the results suggest ourability to detect smells is degrading, more studies are needed to better understand the evolution of human scent receptors.

It sheds light on a long debate in human and primate evolutionthe extent to which sight has tended to replace smell over the last few million years, says Matthew Cobb of the University of Manchester and author of Smell: A Very Short Introduction, to the Guardian. There are another 400 or so receptors to study, and the vast majority of our responses to odors remain a mystery.

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Humans' Sense of Smell May Be Worse Than Our Primate Ancestors' - Smithsonian

Chicago, Feb. 07, 2022 (GLOBE NEWSWIRE) -- The artificial intelligence in genomics market is expected to grow at a CAGR of over 48.44% during the period 20212027.

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Artificial Intelligence in Genomics Market Dynamics

More recently, the formation of DNA biobanks, which are collaborative repositories of genome sequences, and the growth of direct-to-consumer genetics testing companies such as 23andMe have increased the explosion of genomic data. Top healthcare investors, such as Sequoia Capital and Deerfield Management, acknowledge that data has unlocked considerable commercial opportunities across healthcare verticals. In 2017, liquid biopsy company GRAIL raised USD 914 million in its Series B round led by Smart Money VC ARCH Venture Partners and including Johnson & Johnson to continue product development and validation for its early-stage cancer detection blood tests. A number of genomic-focused companies have shown favorable returns. This can be exemplified by the MSCI ACWI Genomic Innovation Index, which has overtaken the standard by nearly 50% since 2013.

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Artificial Intelligence in Genomics Market Geography

North America accounted for a share of 45.19% in the global AI in genomics market in 2021. Post the human genome project, and multiple initiatives have been made across countries such as the US to sequence numerous patients with new targeted diseases. Also, with technological advances the cost of sequencing has been reduced in the market. This has increased patient interest in personal genomic sequencing for future personalized treatments, lifestyle, nutritional study, and other genomics studies. North America is one of the largest AI markets across the globe and is leading the way for other countries to increase the use of AI in the field of genomics and diagnosis in the medical sector. Countries such as Canada and the US are the major revenue contributors in North America. The AI in genomics market is expected to increase in North America due to the growing adoption of AI in genome sequencing and rising awareness among the regional pharma and biotech companies.

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Artificial Intelligence in Genomics Market Size to Reach Revenues of USD 5724.45 Million by 2027 - GlobeNewswire

DetailsCategory: DNA RNA and CellsPublished on Tuesday, 08 February 2022 16:28Hits: 278

- Data presented at the 18th Annual WORLDSymposiumTM 2022 -

TOKYO, Japan I February 7, 2022 I Astellas Pharma Inc. (TSE: 4503, President and CEO: Kenji Yasukawa, Ph.D., "Astellas") today announced positive interim safety data from FORTIS, the Phase I/II clinical trial evaluating AT845, an investigational adeno-associated virus (AAV) gene replacement therapy to deliver a functional alpha-glucosidase (GAA) gene to express acid alpha-glucosidase (GAA) directly in muscle cells in adults with Late-Onset Pompe Disease (LOPD) (Presentation & Poster: 206).

Pompe disease, a rare, severe, autosomal recessive metabolic disease characterized by progressive muscular degeneration, results from a mutation in the GAA gene that interferes with the production or function of the GAA protein. GAA is responsible for metabolizing glycogen, and dysfunction or absence of this protein results in the accumulation of glycogen, primarily in the skeletal and cardiac muscles, where it causes damage to tissue structure and function. Currently, the only approved treatment for Pompe disease is enzyme replacement therapy (ERT), which is delivered via chronic intravenous infusions every two weeks and relies solely on tissue uptake of GAA from plasma.

"There is significant unmet need for patients with Pompe diseasedue to the short half-life, inefficient uptake in the key tissues affected by the disease and the immunogenicity of ERT," said Tahseen Mozaffar, M.D., Professor of Neurology at UC Irvine. "AT845 has the potential to be a best-in-class approach as a muscle-directed gene therapy using an AAV8 capsid serotype. It is being investigated to determine whether it can deliver a functional GAA gene that is efficiently transduced to express GAA directly in tissues affected by the disease, including skeletal and cardiac muscle."

FORTIS is an ongoing multicenter, open-label, ascending dose Phase I/II first-in-human clinical trial to determine if AT845 is safe and tolerable in adults with LOPD. Enrolled participants receive a one-time peripheral intravenous infusion of AT845, followed by one year of frequent monitoring of safety, clinical and biochemical endpoints including GAA activity and protein level in muscle and four additional years of long-term safety monitoring. The primary endpoints of the trial are safety and tolerability, as well as efficacy measures, including change in muscle GAA protein expression and enzyme activity from baseline. Secondary endpoints evaluate improvements in respiratory, endurance and quality of life measures.

As of the December 3, 2021 data cut-off date, four participants have been enrolled in FORTIS, with two participants dosed at 3 x 1013 vg/kg (Cohort 1) and two participants dosed at 6 x 1013 vg/kg (Cohort 2). The reported data includes interim safety and tolerability assessments, as well as up to 24 weeks of follow-up for the two participants in Cohort 1 and preliminary data from the two participants in Cohort 2.

"We are pleased that AT845 has been well-tolerated so far in the four adults with LOPD who have received treatment," said Weston Miller, M.D., Senior Medical Director, Clinical Development at AstellasGene Therapies. "In the two participants in Cohort 1 with follow-up duration through week 24 after dosing, AT845 demonstrated an encouraging safety profile. Importantly, there have been no serious adverse events reported following dosing in any of the four participants as of the time of the data cut. One participant experienced elevated transaminases, which is considered a common immune-mediated treatment response based on the time of onset after dosing, its presentation during steroid taper initiation and its reversal with steroid re-initiation. These safety data are encouraging, and the program continues to enroll participants."

With the establishment of the Astellas Gene Therapies Center of Excellence following the 2020 acquisition of Audentes Therapeutics Inc., Astellas is a leader in genetic medicines, working alongside its world-renowned partners to build a portfolio of potentially life-changing gene therapies. Astellas strives to identify, develop and deliver transformative therapies for patients with genetic diseases who currently have few or no effective treatment options.

About Pompe DiseasePompe disease is a rare, severe, autosomal recessive metabolic disease characterized by progressive muscular degeneration. The overall incidence is estimated to be approximately 1 in 40,000 births,ialthough frequency and disease progression varies with age of onset, ethnicity and geography.iiThe disease is caused by mutations in the alpha-glucosidase (GAA) genethat prevent the production and function of a protein called acid alpha-glucosidase (GAA). GAA is responsible for metabolizing glycogen, and dysfunction or absence of this protein results in the accumulation of glycogen in tissues, primarily in the skeletal and cardiac muscles, where it causes damage to tissue structure and function. Currently, the only approved treatment for Pompe is enzyme replacement therapy (ERT), which is a chronic treatment delivered in bi-weekly infusions and relies solely on tissue uptake of GAA from plasma.

About AT845 for the treatment of Late-Onset Pompe Disease (LOPD)Astellas is developing AT845, a novel gene replacement therapy using an AAV8 vector, under a cardiac- and skeletal muscle-specific promotor, to deliver a functional copy of the GAA gene, for the treatment of Late-Onset Pompe Disease (LOPD). AT845 is being investigated to determine whether it can deliver a functional GAA gene that is efficiently transduced to express GAA directly in tissues affected by the disease, including skeletal and cardiac muscle.

About FORTISFORTIS is an ongoing multicenter, open-label, ascending dose Phase I/II first-in-human clinical trial to determine if AT845 is safe and tolerable in adults with Late-Onset Pompe Disease (LOPD). The primary endpoints of the trial are safety and tolerability, as well as efficacy measures, including change in muscle GAA protein expression and enzyme activity from baseline. Secondary endpoints evaluate improvements in respiratory, endurance and quality of life measures.

About AstellasAstellas Pharma Inc. is a pharmaceutical company conducting business in more than 70 countries around the world. We are promoting the Focus Area Approach that is designed to identify opportunities for the continuous creation of new drugs to address diseases with high unmet medical needs by focusing on Biology and Modality. Furthermore, we are also looking beyond our foundational Rx focus to create Rx+ healthcare solutions that combine our expertise and knowledge with cutting-edge technology in different fields of external partners. Through these efforts, Astellas stands on the forefront of healthcare change to turn innovative science into value for patients. For more information, please visit our website at https://www.astellas.com/en.

About Astellas Gene TherapiesAstellas integrated its wholly owned subsidiary, Audentes Therapeutics, Inc., as of April 1, 2021 and established "Astellas Gene Therapies" within the organization as an Astellas Center of Excellence to develop genetic medicines with the potential to deliver transformative value for patients. Based on an innovative scientific approach and industry leading internal manufacturing capability and expertise, we are currently exploring three gene therapy modalities: gene replacement, exon skipping gene therapy, and vectorized RNA knockdown and hope to also advance additional Astellas gene therapy programs toward clinical investigation. We are based in San Francisco, with manufacturing and laboratory facilities in South San Francisco and Sanford, North Carolina.

iKishnani, PS, et al. Pompe disease diagnosis and management guideline. Genetics in medicine: official journal of the American College of Medical Genetics, 2006. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3110959/ii Ausems MG, et al. Frequency of glycogen storage disease type II in The Netherlands: implications for diagnosis and genetic counselling. European Journal of Human Genetics, 1999. Available from: https://www.nature.com/articles/5200367.pdf?origin=ppub; Lin CY, et al. Pompe's disease in Chinese and prenatal diagnosis by determination of alpha-glucosidase activity. Journal of Inherited Metabolic Disease, 1987. Available from: https://pubmed.ncbi.nlm.nih.gov/3106710/; Hirschhorn R, et al. Pediatric Research, 2004; Bashan N, et al. Glycogen storage disease type II in Israel. Israel Journal of Medical Sciences, 1988. Available from: https://europepmc.org/article/med/3132435; Meikle PJ, et al. Prevalence of Lysosomal Storage Disorders. JAMA, 1999. Available from: https://jamanetwork.com/journals/jama/article-abstract/188380

SOURCE: Astellas Pharma

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Astellas Announces Positive Safety Data from the FORTIS Study of AT845 in Adults with Late-Onset Pompe Disease | DNA RNA and Cells | News Channels -...