At World Stem Cell Summit: Why results in trials repairing hearts are so uneven

Just as no two people are the same, neither are the cells in their bone marrow, the most common source of stem cells in clinical trials trying to repair damage after a heart attack. Doris Taylor of the Texas Heart Institute in Houston, which is just a couple hours drive from the site of this year’s World Stem Cell Summit in San Antonio, gave a key note address this morning that offered some good reasons for the variable and often disappointing results in those trials, as well as some ways to improve on those results.

THI's Dr. Doris Taylor

THI’s Dr. Doris Taylor

The cells given in a transplant derived from the patient’s own bone marrow contain just a few percent stem cells and a mix of adult cells, but for both the stem and adult cells the mix is highly variable. Taylor said that in essence we are giving each patient a different drug. She discussed a series of early clinical trials in which cell samples from each patient were banked at the National Heart and Lung and Blood Institute. There they could do genetic and other analysis on the cells and compare that data with how each individual patient faired.

In looking at the few patients in each trial that did better on any one of three measures of improved heart function, they were indeed able to find certain markers that predicted better outcome. In particular they looked at “triple responders,” those who improved in all three measures of heart function. They found there were both certain types of adult cells and certain types of stem cells that seemed to result in improved heart health.

They also found that two of the strongest predictors were gender and age. Women generally develop degenerative diseases of aging like heart disease at an older age than men and since many consider aging to be a failure of our adult stem cells, it would make sense that women have healthier stem cells.

Taylor went on to discuss ways to use this knowledge to improve therapy outcomes. One way would be to select for the more potent cells identified in the NHLBI analysis. She mentioned a couple trials that did show better outcomes using cells derived from heart tissue. One of those is work that CIRM funds at Cedars-Sinai in Los Angeles.

Another option is replace the whole heart and she closed with a review of what is probably her best-known work, trying to just that. In rats and pigs, she has taken donor hearts and used soap-like solutions to wash away the living cells so that all that is left behind are the proteins and sugars that make of the matrix between cells. She then repopulates the scaffolds that still have the outlines of the chambers of the heart and the blood vessels that feed them, with cells from the recipient animal. She has achieved partially functional organs but not fully functional ones. She—along with other teams around the world—is working on the remaining hurdles to get a heart suitable for transplant.

Don Gibbons

CIRM-Funded Scripps Team Replicates Pain in a Lab Dish; Seeks New Treatments for Chronic Sufferers

Pain hurts but it also protects. Thanks to nerve cells called sensory neurons, which weave their nerve fibers throughout our skin and other tissues, we are alerted to dangerous events like touching a hot plate or even to the sense of having a full bladder.

However, trauma such as a spinal cord injury or diseases like HIV and diabetes can damage sensory neurons and cause chronic pain that debilitates rather than protects those affected. Sadly, conventional pain treatments are usually not effective for the stinging, burning, tingling and numbness associated with this type of pain. Clearly, new innovations are needed.

baldwin_3

These induced sensory neurons could be useful in the testing of potential new therapies for pain, itch and related conditions. Credit: Baldwin Lab, The Scripps Research Institute

Last week, a CIRM-funded research team from The Scripps Research Institute, reported in Nature Neuroscience that they developed a technique, which induces human skin cells to transform into sensory neurons in a petri dish. Up until now, the field mostly relied on mouse studies due to the difficulty of collecting and growing human sensory neurons in the lab. This may explain the lack of success in clinical trials for treating chronic pain. As co-lead author Joel Blanchard, a PhD candidate in Kristin Baldwin’s laboratory, stated in the institute’s press release:

“Mouse models don’t represent the full diversity of the human response. [With these human sensory neurons] we can start to understand how individuals respond uniquely to pain, cold, itch and so on.”

Kevin Eade, research associate, and Joel Blanchard, graduate student, co-lead authors of the report  Credit: Cindy Brauer, The Scripps Research Institute

Kevin Eade, research associate, and Joel Blanchard, graduate student, co-lead authors of the report. Credit: Cindy Brauer, The Scripps Research Institute

To generate the nerve cells, the Baldwin research team inserted, into human skin cells, a combination of genes known to produce proteins that are key controllers of sensory neuron function. The resulting cells had the appearance of sensory neurons and responded appropriately when exposed to heat in the form of the active ingredient in chili peppers as well as activating a cold response when exposed to menthol. Adding more confidence to these results, an independent research team from the Harvard Stem Cell Institute reported in the same Nature Neuroscience   issue and in a press release that they too had successfully generated human sensory neurons from skin cells.

This direct reprogramming of one cell type directly into another is a variant of the induced pluripotent stem cell (iPS) technique in which a cell, often skin, is first reprogrammed into an embryonic stem cell-like state and then coaxed to form into virtually any cell type of the body.

Now that the Baldwin lab has nailed down the recipe for making human sensory neurons, they now can seek out treatments to bring relief to chronic pain sufferers. Dr. Baldwin looks forward to this future work:

Kristin Baldwin, Associate Professor Department of Molecular and Cellular Neuroscience. Credit: The Scripps Research Institute

Kristin Baldwin
Associate Professor
Credit: The Scripps Research Institute

“This method is rapid, robust and scalable. Therefore we hope that these induced sensory neurons will allow our group and others to identify new compounds that block pain and itch and to better understand and treat neurodegenerative disease and spinal cord injury.”

Watch the short video below to hear from a pioneer of direct reprogramming of nerve cells, CIRM grantee Marius Wernig of Stanford University:

Searching for a Cure for HIV/AIDS: Stem Cells and World AIDS Day

World-AIDS-Day

It’s been 26 years since the first World AIDS Day was held in 1988—and the progress that the international scientific community has made towards eradicating the disease has been unparalleled. But there is much more work to be done.

One of the most promising areas of HIV/AIDS research has been in the field of regenerative medicine. As you observe World AIDS Day today, we invite you to take a look at some recent advances from CIRM-funded scientists and programs that are well on their way to finding ways to slow, halt and prevent the spread of HIV/AIDS:

Calimmune’s stem cell gene modification study continues to enroll patients, show promise:
Calimmune Approved to Treat Second Group in HIV Stem Cell Gene Modification Study

Is a cure for HIV/AIDS possible? Last year’s public forum discusses the latest on HIV cure research:


Town Hall: HIV Cure Research

The Stem Cell Agency’s HIV/AIDS Fact Sheet summarizes the latest advances in regenerative medicine to slow the spread of the disease.

And for more on World AIDS Day, follow #WorldAIDSDay on Twitter and visit WorldAIDSDay.org.

Using stem cells paves new approach to treating a blistering skin disease

Imagine a child not being able to run or jump or just roll around, for fear that any movement could strip away their skin and leave them with open, painful wounds. That’s what life is like for children with a nasty genetic disease called epidermolysis bullosa or EB. The slightest touch can cause their skin to peel off. People with the disease often die in their late teens or early 20’s from skin cancer, caused by repeated cycles of skin wounding and healing.

Now Stanford researchers, funded by the stem cell agency, have found a way to correct the faulty gene and grow healthy skin, a technique that could completely change the lives of children with EB. This new approach, which the researchers call “therapeutic reprogramming”, is reported in the journal Science Translational Medicine

In the study the researchers took skin cells from patients with EB and reprogrammed them to become induced pluripotent stem (iPS) cells that have the ability to become any of the other cells in the body. They then replaced the faulty gene that caused that particular form of EB and then turned the cells into keratinocytes, the cells that make up most of our outer layer of skin. When they grafted these cells onto the back of laboratory mice they grew into normal human skin.

In a news release about the work, Dr. Anthony Oro, one of the senior authors of the paper, says the work represents a completely different approach to treating EB.

“Normally, treatment has been confined to surgical approaches to repair damaged skin, or medical approaches to prevent and repair damage. But by replacing the faulty gene with a correct version in stem cells, and then converting those corrected stem cells to keratinocytes, we have the possibility of achieving a permanent fix — replacing damaged areas with healthy, perfectly matched skin grafts.”

One of the key words in that quote is “healthy”. Because the skin cells that they got from the patient probably already included some that had a skin cancer-causing mutation, the researchers carefully screened the cells to make sure they removed any that looked suspicious.

Oro says tests showed the resulting skin from these iPS cells was very similar to human skin made from normal keratinocytes.

“The most difficult part of this procedure is to show not just that you can make keratinocytes from the corrected stem cells, but that you can then use them to make graftable skin. What we’d love to do is to be able to give patients healthy skin grafts on the areas that they bang a lot, such as hands and feet and elbows — those places that don’t heal well. That alone would significantly improve our patients’ lives. We don’t know how long these grafts might last in humans; we may need some improvements. But I think we’re getting very close.”

Having seen that this works in mice the team are now eager to see if they can replicate their results in people. With CIRM support they have already been working with the Food and Drug Administration (FDA) to pave the way for that to happen. Dr. Marius Wernig, one of the senior authors of the paper, says that focus on patients is driving their work:

“CIRM made sure that we were always keeping in mind the need to translate our results to the clinic. Now we’ve shown that this approach that we call ‘therapeutic reprogramming’ works well with human cells. We can indeed take skin cells from people with epidermolysis bullosa, convert them to iPS cells, replace the faulty collagen 7 gene with a new copy, and then finally convert these cells to keratinocytes to generate human skin. It is almost like a fountain of youth that, in principle, produces an endless supply of new, healthy skin from a patient’s own cells.”

Speak Friend and Enter: How Cells Let the Right Travelers through their Doors

For decades, it’s been a molecular mystery that scientists were seemingly unable to solve: how do large molecules pass through the cell and into the nucleus, while others half their size remain stranded outside?

These are nuclear pores imaged by atomic force microscopy, appearing as a craterlike landscape in which each crater corresponds to a pore of ~100 nm diameter. [Credit: UCL]

Nuclear pores imaged by atomic force microscopy, appearing as a crater-like landscape in which each crater corresponds to a pore of ~100 nm diameter. [Credit: UCL]

But as reported in the latest issue of Nature Nanotechnology, researchers now believe they may have cracked the case. By shedding light on this strange anomaly, University College London (UCL) scientists have opened the door for one day delivering gene therapies directly into the nucleus. With numerous research teams working on ways to merge stem cell therapy and gene therapy, this could be extremely valuable to our field.

Scientists already knew that the membrane that surrounds the cell’s nucleus is ‘punctured’ with millions of tiny holes, known as nuclear pores. Co-lead author Bart Hoogenboom likened the pores to a strange kind of sieve:

“The pores have been to known to act like a sieve that could hold back sugar while letting grains of rice fall through at the same time, but it was not clear how they were able to do that.”

In this study—which used cells taken from frog eggs—Hoogenboom, along with co-lead author Ariberto Fassati, harnessed atomic force microscopy (AFM) to give them a new understanding of how these pores work. Like a blind person moving their fingers to read braille, AFM uses a tiny needle to pass over the nuclear pores in order to measure their shape and structure.

“AFM can reveal far smaller structures than optical microscopes,” said Hoogenboom, “but it’s feeling more than seeing. The trick is to press hard enough to feel the shape and the hardness of the sample, but not so hard that you break it. [In this study], we used it to successfully probe the membrane…to reveal the structure of the pores.”

And what they found, adds Fassati, offered an explanation for how these pores worked:

“We found that the proteins in the center of the pores tangle together just tightly enough to form a barrier—like a clump of spaghetti. Large molecules can only pass through [the pores] when accompanied by chaperone molecules. These chaperones, called nuclear transport receptors, have the property of lubricating the [spaghetti] strands and relaxing the barrier, letting the larger molecules through.”

Astoundingly, Fassati said that this process happens upwards of several thousand times per second.

These results are exciting not only for solving a long-standing mystery, but also for pointing to new ways of delivering gene therapies.

As evidenced by recent clinical advances in conditions such as sickle cell disease and SCID (‘bubble baby’ disease), gene therapy represents a promising way to treat—and even cure—patients. Hoogenboom and Fassati are optimistic that their team’s discovery could lead further refinements to gene therapy techniques.

Said Fassati, “It may be possible to improve the design of current mechanisms for delivering gene therapy to better cross the nuclear pores and deliver their therapeutic genes into the nucleus.”

Shape-Shifting Cells Drive Bone Healing; Point to New Method of Correcting Bone Deformities

There’s a time to grow and a time to heal—and the cells that make up our bone and cartilage have impeccable timing. During childhood and adolescence, these cells work to grow the bones longer and stronger. Once we’ve reached adulthood, they shift focus to repair and healing.

New research may help doctors treat craniofacial abnormalities while the patient is still growing—rather than having to wait until adulthood.

New research may help doctors treat craniofacial abnormalities while the patient is still growing—rather than having to wait until adulthood.

This is part of why children with bone deformities are often forced to wait until adulthood—until their bones stop growing—before their condition can be corrected.

Another part of the reason behind the agonizing wait is that scientists still don’t know exactly how this transition in bone cells, from a focus on growing to a focus on healing, even happens.

But new research out of the University of Michigan (UM) is well on its way to changing that.

In findings published today in Nature Cell Biology, Noriaki Ono (a UM assistant professor of dentistry) and his team announce the discovery of a subset of cartilage-making cells that take on new duties during the transition from adolescence into adulthood.

Previously, scientists had thought that these cartilage-making cells, known as chondrocytes, die once the bones stopped growing. But these new findings by Ono and his team showed that is not the case—not all chondrocytes bite the dust. Instead, they literally transform themselves from growing bone, to healing it.

The fact that some chondrocytes persist through to adulthood may mean that they can be selectively targeted to correct bone deformities in younger patients. As Ono explained in more detail:

“Up until now, the cells that drive this bone growth have not been understood very well. As an orthodontist myself, I have special interest in this aspect, especially for finding a cure for severe bone deformities in the faces of children. If we can find a way to make bones that continue to grow alongside the child, maybe we should be able to put these pieces of growing bones back into children and make their faces look much better than they do.”

Taking stock: ten years of the stem cell agency, progress and promise for the future

Under some circumstances ten years can seem like a lifetime. But when lives are at stake, ten years can fly by in a flash.

Ten years ago the people of California created the stem cell agency when they overwhelmingly approved Proposition 71, giving us $3 billion to fund and support stem cell research in the state.

In 2004 stem cell science held enormous potential but the field was still quite young. Back then the biology of the cells was not well understood, and our ability to convert stem cells into other cell types for potential therapies was limited. Today, less than 8 years after we actually started funding research, we have ten projects that are expected to be approved for clinical trials by the end of the year, including work in heart disease and cancer, HIV/AIDS and diabetes. So clearly great progress has been made.

Dean Carmen Puliafito and the panel at the Tenth Anniversary event at USC

Dean Carmen Puliafito and the panel at the Tenth Anniversary event at USC

Yesterday we held an event at the University of Southern California (USC) to mark those ten years, to chart where we have come from, and to look to where we are going. It was a gathering of all those who have, as they say, skin in the game: researchers, patients and patient advocates.

The event was held at the Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research. As Dr. Carmen Puliafito, Dean of USC’s Keck School of Medicine noted, without CIRM the building would not even exist.

“With this funding, our researchers, and researchers in 11 other facilities throughout the state, gained a dedicated space to hunt for cures for some of the most pernicious diseases in the world, including heart disease, stroke, cancer, diabetes, Alzheimer’s and Parkinson’s disease.”

Dr. Dhruv Sareen from Cedars-Sinai praised CIRM for creating a whole new industry in the state:

“What Silicon Valley has done for technology, CIRM is doing for stem cell research in California.”

One of the beneficiaries of that new industry has been ViaCyte, a San Diego-based company that is now in clinical trials with a small implantable device containing stem cell-derived cells to treat type 1 diabetes. ViaCyte’s Dr. Eugene Brandon said without CIRM none of that would have been possible.

“In 2008 it was extremely hard for a small biotech company to get funding for the kind of work we were doing. Without that support, without that funding from CIRM, I don’t know where this work would be today.”

As with everything we do, at the heart of it are the patients. Fred Lesikar says when he had a massive heart attack and woke up in the hospital his nurse told him about a measure they use to determine the scale of the attack. When he asked how big his attack had been, she replied, “I’ve never seen numbers that large before. Ever.”

Fred told of leaving the hospital a diminished person, unable to do most basic things because his heart had been so badly damaged. But after getting a stem cell-based therapy using his own heart cells he is now as active as ever, something he says doesn’t just affect him.

“It’s not just patients who benefit from these treatments, families do too. It changes the life of the patient, and the lives of all those around them. I feel like I’m back to normal and I’m so grateful for CIRM and Cedars-Sinai for helping me get here.”

The team behind that approach, based at Cedars-Sinai, is now in a much larger clinical trial and we are funding it.

The last word in the event was left to Bob Klein, who led the drive to get Proposition 71 passed and who was the agency’s first Chair. He said looking at what has happened in the last ten years: “it is beyond what I could have imagined.”

Bob noted that the field has not been without its challenges and problems to overcome, and that more challenges and problems almost certainly lie in the future:

“But the genius of the people of this state is reflected in their commitment to this cause, and we should all be eternally grateful for their vision in supporting research that will save and transform people’s lives.”

10 Years/10 Therapies: 10 Years after its Founding CIRM will have 10 Therapies Approved for Clinical Trials

In 2004, when 59 percent of California voters approved the creation of CIRM, our state embarked on an unprecedented experiment: providing concentrated funding to a new, promising area of research. The goal: accelerate the process of getting therapies to patients, especially those with unmet medical needs.

Having 10 potential treatments expected to be approved for clinical trials by the end of this year is no small feat. Indeed, it is viewed by many in the industry as a clear acceleration of the normal pace of discovery. Here are our first 10 treatments to be approved for testing in patients.

HIV/AIDS. The company Calimmune is genetically modifying patients’ own blood-forming stem cells so that they can produce immune cells—the ones normally destroyed by the virus—that cannot be infected by the virus. It is hoped this will allow the patients to clear their systems of the virus, effectively curing the disease.

Spinal cord injury patient advocate Katie Sharify is optimistic about the latest clinical trial led by Asterias Biotherapeutics.

Spinal cord injury patient advocate Katie Sharify is optimistic about the clinical trial led by Asterias Biotherapeutics.

Spinal Cord Injury. The company Asterias Biotherapeutics uses cells derived from embryonic stem cells to heal the spinal cord at the site of injury. They mature the stem cells into cells called oligodendrocyte precursor cells that are injected at the site of injury where it is hoped they can repair the insulating layer, called myelin, that normally protects the nerves in the spinal cord.

Heart Disease. The company Capricor is using donor cells derived from heart stem cells to treat patients developing heart failure after a heart attack. In early studies the cells appear to reduce scar tissue, promote blood vessel growth and improve heart function.

Solid Tumors. A team at the University of California, Los Angeles, has developed a drug that seeks out and destroys cancer stem cells, which are considered by many to be the reason cancers resist treatment and recur. It is believed that eliminating the cancer stem cells may lead to long-term cures.

Leukemia. A team at the University of California, San Diego, is using a protein called an antibody to target cancer stem cells. The antibody senses and attaches to a protein on the surface of cancer stem cells. That disables the protein, which slows the growth of the leukemia and makes it more vulnerable to other anti-cancer drugs.

Sickle Cell Anemia. A team at the University of California, Los Angeles, is genetically modifying a patient’s own blood stem cells so they will produce a correct version of hemoglobin, the oxygen carrying protein that is mutated in these patients, which causes an abnormal sickle-like shape to the red blood cells. These misshapen cells lead to dangerous blood clots and debilitating pain The genetically modified stem cells will be given back to the patient to create a new sickle cell-free blood supply.

Solid Tumors. A team at Stanford University is using a molecule known as an antibody to target cancer stem cells. This antibody can recognize a protein the cancer stem cells carry on their cell surface. The cancer cells use that protein to evade the component of our immune system that routinely destroys tumors. By disabling this protein the team hopes to empower the body’s own immune system to attack and destroy the cancer stem cells.

Diabetes. The company Viacyte is growing cells in a permeable pouch that when implanted under the skin can sense blood sugar and produce the levels of insulin needed to eliminate the symptoms of diabetes. They start with embryonic stem cells, mature them part way to becoming pancreas tissues and insert them into the permeable pouch. When transplanted in the patient, the cells fully develop into the cells needed for proper metabolism of sugar and restore it to a healthy level.

HIV/AIDS. A team at The City of Hope is genetically modifying patients’ own blood-forming stem cells so that they can produce immune cells—the ones normally destroyed by the virus—that cannot be infected by the virus. It is hoped this will allow the patients to clear their systems of the virus, effectively curing the disease

Blindness. A team at the University of Southern California is using cells derived from embryonic stem cell and a scaffold to replace cells damaged in Age-related Macular Degeneration (AMD), the leading cause of blindness in the elderly. The therapy starts with embryonic stem cells that have been matured into a type of cell lost in AMD and places them on a single layer synthetic scaffold. This sheet of cells is inserted surgically into the back of the eye to replace the damaged cells that are needed to maintain healthy photoreceptors in the retina.

UCLA team cures infants of often-fatal “bubble baby” disease by inserting gene in their stem cells; sickle cell disease is next target

Poopy diapers, ear-splitting cries, and sleepless nights: sure, the first few weeks of parenthood are grueling but those other moments of cuddling and kissing your little baby are pure bliss.

The bubble boy.  Born in 1971 with SCID, David Vetter lived in a sterile bubble to avoid outside germs that could kill him. He died in 1984 at 12 due to complications from a bone marrow transplant. [Credit: Baylor College of Medicine Archives]

The bubble boy. Born in 1971 with SCID, David Vetter lived in a sterile bubble to avoid outside germs that could kill him. He died in 1984 at 12 due to complications from a bone marrow transplant. [Credit: Baylor College of Medicine Archives]

That wasn’t the case for Alysia and Christian Padilla-Vacarro of Corona, California. Close contact with their infant daughter Evangelina, born in 2012, was off limits. She was diagnosed with a genetic disease that left her with no immune system and no ability to fight off infections so even a minor cold could kill her.

Evangelina was born with Severe Combined Immunodeficiency (SCID) also called “bubble baby” disease, a term coined in the 1970s when the only way to manage the disease was isolating the child in a super clean environment to avoid exposure to germs. Bone marrow transplants from a matched sibling offer a cure but many kids don’t have a match, which makes a transplant very risky. Sadly, many SCID infants die within the first year of life.

Until now, that is.

Today, a UCLA research team led by Donald Kohn, M.D., announced a stunning breakthrough cure that saved Evangelina’s life and all 18 children who have so far participated in the clinical trial. Kohn—the director of UCLA’s Human Gene Medicine Program—described the treatment strategy in a video interview with CIRM (watch the video below):

“We collect some of the baby’s own bone marrow, isolate the [blood] stem cells, add the gene that they’re missing that their immune system needs and then transplant the cells back to them. “

Inserting the missing gene, called ADA, into the blood stem cells restores the cells’ ability to produce a healthy immune system. And since the cells originally came from the infant, there’s no worry about the possible life-threatening complications from receiving non-matched donor cells.

This breakthrough didn’t occur overnight. Kohn and colleagues have been plugging away for over twenty years carrying out trials, observing their limitations and going back to lab to improve the technology. Their dedication has paid off. As Kohn states in a press release:

“All of the children with SCID that I have treated in these stem cell clinical trials would have died in a year or less without this gene therapy, instead they are all thriving with fully functioning immune systems.”

Alysia Padilla-Vacarro and daughter Evangelina on the day of her gene therapy treatment. Evangelina, now two years old, has had her immune system restored and lives a healthy and normal life. [Credit: UCLA Broad Center of Regenerative Medicine and Stem Cell Research.]

Alysia Padilla-Vacarro and daughter Evangelina on the day of her gene therapy treatment. Evangelina, now two years old, has had her immune system restored and lives a healthy and normal life. [Credit: UCLA Broad Center of Regenerative Medicine and Stem Cell Research.]

For the Padilla-Vacarro family, the dark days after Evangelina’s grave diagnosis have given way to a bright future. Alysia, Evangelina’s mom, poignantly recalled her daughter’s initial recovery:

”It was only around six weeks after the procedure when Dr. Kohn told us Evangelina can finally be taken outside. To finally kiss your child on the lips, to hold her, it’s impossible to describe what a gift that is. I gave birth to my daughter, but Dr. Kohn gave my baby life.”

The team’s next step is to get approval by the Food and Drug Administration (FDA) to provide this treatment to all SCID infants missing the ADA gene.

At the same time, Kohn and colleagues are adapting this treatment approach to cure sickle cell disease, a genetic disease that leads to sickle shaped red blood cells. These misshapen cells are prone to clumping causing debilitating pain, risk of stroke, organ damage and a shortened life span. CIRM is providing over $13 million in funding to support the UCLA team’s clinical trial set to start early next year.

For more information about CIRM-funded sickle cell disease research, visit our fact sheet.

Entrepreneurship and Education

Guest author Neil Littman is CIRM’s Business Development Officer.

CIRM works closely with UCSF on a number of initiatives, from providing funding to academic investigators to jointly hosting events such as the recent CIRM Showcase with J-Labs held at the Mission Bay campus.

Beyond our joint initiatives, UCSF also provides many other valuable resources and educational opportunities to the life sciences community in the Bay Area. For instance, I was a mentor in UCSF’s “Idea to IPO” class which focused on helping students translate concepts into a commercializable product and viable business.

Another opportunity that may be of interest to all you budding entrepreneurs is UCSF’s Lean LaunchPad course, which kicks off in January (application deadline is Nov 19th). The course teaches…

“scientists and clinicians how to assess whether the idea or technology they have can serve as the basis of a business. The focus is on the marketplace where you must validate that your idea has value in order to move into the commercial world.”

See more at: Lean Launchpad for Life Sciences & Healthcare.

The course is being run out of the Entrepreneurship Center at UCSF, which is a division of the UCSF Office of Innovation, Technology & Alliances (ITA).