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).

More Than Meets the Eye: Protein that Keeps Cancer in Check also Plays Direct Role in Stem Cell Biology, a Stanford Study Finds.

Here’s a startling fact: the retinoblastoma protein —Rb, for short — is defective or missing in nearly all cancers.

Rb is called a tumor suppressor because it prevents excessive cell growth by acting as a crucial traffic stop for the cell cycle, a process that controls the timing for a cell to divide and multiply. Without a working Rb protein, that traffic barrier on cell division is effectively removed, allowing unrestricted cell growth and a path towards cancer.

Retinoblastoma - a known road block to cancer growth also inhibits a stem cell's capacity to change into any cell type

Retinoblastoma – a known road block to cancer growth also inhibits a stem cell’s capacity to change into any cell type

The Rb gene was cloned over two decades ago and its link to cancer has been known for years. But today in Cell Stem Cell, CIRM-funded scientists at Stanford University report an unexpected finding: Rb protein also inhibits a stem cell’s pluripotency, or it’s capacity to become any type of cell in the body. Julien Sage, a senior author of the report, described this new facet to Rb in a press release:

“We were very surprised to see that retinoblastoma directly connects control of the cell cycle with pluripotency. This is a completely new idea as to how retinoblastoma functions.”

The research team uncovered Rb’s versatility in experiments using the induced pluripotent stem cell (iPS) technique in which adult cells, such as a skin, are reprogrammed to an embryonic stem cell-like state that, in turn, can be transformed into any cell type.

Creating iPS cells is notoriously slow and inefficient. However, the Stanford scientists found that cells without Rb were much easier and faster to convert to iPS than cells with normal Rb. And when Rb protein levels in the cells were boosted, it was much more difficult to make the iPS cells — suggesting that the presence of Rb was encouraging the skin cells to remain skin and to resist reprogramming into an iPS cell. As Marius Wernig, the other senior author, sums it up:

“The loss of Rb appears to directly change a cell’s identity. Without the protein, the cell is much more developmentally fluid and is easier to reprogram into an iPS cell.”

And Dr. Sage further points out that:

“The process of creating iPS cells from fully differentiated, or specialized, cells is in many ways very similar to what happens when a cell becomes cancerous.”

So now that the team has established the Rb protein’s direct link between stem cell and cancer biology, they stand at unique vantage point to gain new insights on the inner workings of both, such as better iPS methods and new cancer therapy targets.

To hear about more aspects of Marius Wernig’s research, watch his 30 second elevator pitch below:

Creating a Genetic Model for Autism, with a Little Help from the Tooth Fairy

One of the most complex aspects of autism is that it is not one disease—but many. Known more accurately as the autism spectrum disorder, or ASD, experts have long been trying to tease apart the various ways in which the condition manifests in children, with limited success.

But now, using the latest stem cell technology, scientists at the University of California, San Diego (UCSD) have identified a gene associated with Rett Syndrome—a rare form of autism almost exclusively seen in girls. And in so doing, the team has made the startling discovery that the many types of autism may be linked by common molecular pathways.

The research team, led by UCSD Professor and CIRM grantee Alysson Muotri, explained in a news release how induced pluripotent stem cell, or iPS cell, technology was used to pinpoint a gene associated with Rett Syndrome:

“One can take advantage of genomics to map all mutant genes in the patient and then use their own iPS cells to measure the impact of mutations in relevant cell types. Moreover, the study of brain cells derived from these iPS cells can reveal potential therapeutic drugs tailored to the individual. It is the rise of personalized medicine for mental and neurological disorder.”

iPS cell technology—a process by which scientists transform adult skin cells back into embryonic-like stem cells, after which they can be coaxed into maturing into virtually any type of cell—is a promising way to model diseases at the cellular level. But in order to truly understand what is happening in the brains of people with autism, Muotri and his team needed more samples from autistic individuals—on the order of hundreds or even thousands.

The Tooth Fairy Project allows scientists to gather large quantities of cells from autistic individuals for genomic analysis—simply asking parents to send in a discarded baby tooth.

The Tooth Fairy Project allows scientists to gather large quantities of cells from autistic individuals for genomic analysis—simply by asking parents to send in a discarded baby tooth.

Luckily, Muotri had a little help from the Tooth Fairy.

Or, more accurately, the Tooth Fairy Project, in which parents register for a “Fairy Tooth Kit” that lets them send a discarded baby tooth of their autistic child to researchers. Housed within each baby tooth are cells that can be transformed—with iPS cell technology—into neurons, thus giving the researchers a massive sample size with which to study.

Interestingly, the findings presented here come from the very first tooth to be sent to Muotri. Specifically, the team identified a mutation in the gene TRPC6 was present in children with autism. Additional experiments in animal models revealed that the TRPC6 mutation was indeed associated with abnormal brain cell development and function.

And for their next trick, the team found a way to reverse the mutation’s damaging effects.

By treating the cells with the chemical hyperforin, they were able to restore some normal function to the neurons—offering up a potential therapeutic strategy for treating ASD patients who harbor the TRPC6 mutation.

Drilling down even further, the team found that mutations in another gene called MeCP2, which causes Rett Syndrome, also set off a genetic domino effect that alters the normal function of the TRPC6 gene. Thus connecting this syndrome with other, non-syndromic types of autism.

“Taken together, these findings suggest that TRPC6 is a novel predisposing gene for ASD that may act in a multiple-hit model,” said Muotri. “This is the first study to use iPS cell-derived human neurons to model non-syndromic ASD and illustrate the potential of modeling genetically complex sporadic diseases using such cells.”

Find out more about how stem cell research could help solve the mysteries behind autism in our Autism Fact Sheet.

CIRM Scientists Discover Key to Blood Cells’ Building Blocks

Our bodies generate new blood cells—both red and white blood cells—each and every day. But reproducing that feat in a petri dish has proven far more difficult.

Pictured: sections from zebrafish embryos. Blood vessels are labeled in red, the protein complex that regulates inflammation green and cell nuclei in blue. The arrowhead indicates a potential HSC. The image at bottom right combines all channels. [Credit: UC San Diego School of Medicine]

Pictured: sections from zebrafish embryos. Blood vessels are labeled in red, the protein complex that regulates inflammation green and cell nuclei in blue. The arrowhead indicates a potential HSC. The image at bottom right combines all channels.
[Credit: UC San Diego School of Medicine]

But now, scientists have identified the missing ingredient to producing hematopoietic stem cells, or HSC’s—the type of stem cell that gives rise to all blood and immune cells in the body. The results, published last week in the journal Cell, describe how a newly discovered protein plays a key role in generating HSC’s in the developing embryo—giving scientists a more complete recipe to reproduce these cells in the lab.

The research, which was led by University of California, San Diego (UCSD) professor David Traver and supported by a grant from CIRM, offers renewed hope for the possibility of generating patient-specific blood or immune cells using induced pluripotent stem cell (iPS cell) technology.

As Traver explained in last week’s news release:

“The development of some mature cell lineages from iPS cells, such as cardiac or neural, has been reasonably straightforward, but not with HSCs. This is likely due, at least in part, to not fully understanding all the factors used by the embryo to generate HSCs.”

Indeed, the ability to generate HSCs has long challenged scientists, as outlined in a CIRM workshop from last year. But now, says Traver, they have found a crucial piece to the puzzle.

Specifically, the researchers investigated a signaling protein called tumor necrosis factor alpha—or TNFα for short— a protein known to be important for regulating inflammation and immunity. Previous research by this study’s first author, Raquel Espin-Palazon, and others also discovered it was related to the healthy function of blood vessels during embryonic development.

In this study, Traver, Espin-Palazon and the UCSD drilled down even further—and found that TNFα was required for the normal development of HSCs in the embryo. This surprised the research team, as the young embryo is generally considered to be sterile—with no need for a protein normally charged with regulating immune response to be switched on. Explained Traver:

“There was no expectation that pro-inflammatory signaling would be active at this time or in the blood-forming regions.”

While preliminary, establishing this relationship between TNFα and HSC formation will be a boon to researchers looking for new ways to generate large quantities of healthy, patient-specific red and white blood cells for those patients who so desperately need them.

Learn more about how stem cell technology could help treat blood diseases in our Thalassemia Fact Sheet.

How venture capital became a capital adventure for stem cell agency’s newest Board member

Kathy LaPorte, the newest member of the CIRM Board

Kathy LaPorte, the newest member of the CIRM Board

There’s something fascinating about looking at the arc of a person’s career. So often we start out thinking we are going to be one thing, and over the years we move in a different direction and end up doing something else entirely.

That’s certainly the case with Kathy LaPorte, the newest addition to our governing Board, the Independent Citizens Oversight Committee (ICOC).

Ms. Laporte started out with dreams of being a doctor and, after getting a biology degree at Yale University, she applied to go to medical school at both Stanford and Harvard (she was accepted at both, which tells you something about her ability). But somewhere along the way she realized that being a doctor was not for her and so she started thinking about other directions. The one she ultimately chose was business.

And she went about it in style. After gaining experience with a number of firms she teamed up with some colleagues to start New Leaf Venture Partners, a venture capital firm based in Silicon Valley.

A profile of her in the Silicon Valley Business Journal described her as “smart, thorough and solution-oriented, Ms. LaPorte has spent nearly her entire professional life in venture capital — something of a rarity — and is considered a quick study by those who have worked with her.”

But it’s not just her business acumen that earned her the respect of colleagues and an appointment to our Board by State Treasurer Bill Lockyer. It’s also her experience working in the biotech and healthcare field, evaluating and mentoring later stage biotech companies and early stage medical device and diagnostic companies.

“I’m honored to be joining the Board, and excited about CIRM’s mission to bring new regenerative medicine therapies to patients with chronic diseases,” says Ms. LaPorte. “I hope my experience from 28 years of helping to finance and guide the work of passionate scientists and entrepreneurs, enabling their ideas to get to the people who really need them, will be helpful to the CIRM team.”

In a news release announcing the news, Jonathan Thomas, the Chair of our Board, said:

“We are thrilled to have Kathy join us on the ICOC. As a representative of a life science commercial entity she brings with her a wealth of knowledge and expertise in biotech and business development for healthcare companies and products. Her keen intellect and analytical skills are going to be terrific assets for the Board.”

Ms. LaPorte’s career took a few twists and turns before it led to us, but we’re delighted it brought her here, and we welcome her to the Board.

Stem cell stories that caught our eye: heart repair, epilepsy and comparing cloned and reprogrammed cells

Here are some stem cell stories that caught our eye this past week. Some are groundbreaking science, others are of personal interest to us, and still others are just fun.

Reminding broken hearts how to mend them selves.
After years of tracking down the right genetic buttons a team at the Salk Institute in La Jolla has taught a mammal to do what zebra fish do naturally, repair a severely damaged heart. While all our cells have the genetic code for building whole organs those genes seem to be switched off in all higher animals, but active in some more primitive species like zebra fish and salamanders.

New cells (red) repairing injury in a zebra fish heart.

New cells (red) repairing injury in a zebra fish heart.

Starting a decade ago the researchers measured the gene activity during heart repair in the fish. They found many genes that had their on-off status change during repair. They then looked to see which of those genes had been preserved during evolution to mammal species. They found four genes that were turned off during repair in the fish but were turned on in the mice they were using.

When, with CIRM funding, they inserted genetic signals to turn off those genes in the mice, they saw significant repair of the damaged heart. There are many steps between this advance and getting human hearts to repair them selves—notably finding a way to introduce the genetic signals without using the virus used in this study. HealthCanal picked up the institute’s press release.

Cloned stem cells pretty much like reprogrammed stem cells. In the early days of stem cell research there was a great deal of excitement about the possibility of creating stem cells that genetically match a patient by a process commonly called cloning. This process of taking the genetic storehouse of a cell, the nucleus, and inserting it into a donor egg had been relatively easy in mice. But it turned out quite difficult in humans and was only accomplished last year.

During the years of failed attempts at this process known as nuclear transfer in humans an alternative came into the field. The Nobel prize-winning discovery that you can reprogram any adult cell to act like an embryonic stem cell gave us a new way to create personalized stem cells that genetically match a patient. But ever since that 2008 advance, the research community has fretted over whether those new stem cells called iPS cells really match embryonic stem cells. The iPS cells came from older cells that had lived through many opportunities for mutation and the genetic factors used to reprogram them added further opportunities for mutation.

Researchers at the New York Stem Cell Foundation’s in house lab have now compared the two types of cells with several layers of genetic analysis. They found the same level of mutation in the iPS cells and the cells from nuclear transfer lending some reassurance to the use of iPS cells going forward. HealthCanal ran the foundation’s press release.

A more efficient way to make cloned stem cells. Even though a team in Oregon overcame the obstacles to creating stem cells by nuclear transfer last year, and the feat has been repeated by the New York team above and others, it remains terribly inefficient. So, several groups are working on better ways to make these potentially valuable cells.

A former colleague now at Children’s Hospital, Boston wrote a nice explanation of how researchers are going about making these cloned cells easier in the hospital’s blog, Vector.

Stem cells reduced seizures.
The seizures endured by people with many forms of epilepsy originate from genetic defects in their nerves. So, a team at McClean Hospital outside of Boston implanted healthy nerves grown from embryonic stem cells in mice with genetically linked seizures. Half the mice no longer had seizures and the other half had their seizure frequency reduced.

The type of nerves transplanted are called interneurons, which are known to be the nerves that reduce firing of signals. In epilepsy nerve signals are hyperactive. The team is now working on methods to mature the stem cells into purer populations of just the desired interneurons. ClinicalSpace picked up the hospital’s press release.

Don Gibbons

Unlocking the Wonder Drug’s Secrets: Aspirin Fends Off Colon Cancer by Killing Faulty Intestinal Stem Cells

Over 700,000 people worldwide died from colorectal cancer in 2010, up from 500,000 in 1990, making it the fourth leading cause of cancer death behind lung, stomach and liver.

Remarkably, your household bottle of aspirin – in addition to relieving the common headache – protects against colorectal cancer based on several clinical trials over the past few decades. Though its effect is clear, how exactly aspirin prevents colon cancer has remained murky.

Who cares how it works as long as it saves lives, right?

Ball and stick model of aspirin, the wonder drug: relieves pain and prevents cancer

Ball and stick model of the wonder drug, aspirin. It not only relieves pain but also prevents heart attacks and even cancer.

Well, it turns out that long-term daily use of aspirin carries risks of internal bleeding of the stomach and brain, kidney failure, and certain types of strokes. So unraveling what exactly aspirin does to fend off tumors is an important step to finding new drugs with fewer side effects.

Earlier this week, scientists at University of Pittsburgh Cancer Institute (UPCI) reported that they’ve unlocked the secrets of aspirin’s tumor-killing powers. In their study, published in the Proceedings of the National Academy of Sciences (PNAS), the UPCI team shows that aspirin prevents colon cancer by orchestrating the death of stem cells in the intestine that carry a dangerous mutation.

Most colorectal cancers initially crop up with a mutation in a gene called APC. The APC protein is a so-called tumor suppressor, which acts to keep a lid on any uncontrolled cell division, an early step to tumor growth. So a bad APC gene leads to a faulty APC protein and, in turn, the potential for normal intestinal cells to become cancerous. The intestine has a rich source of stem cells, which are particularly vulnerable to this mutation since stem cells already possess the ability for unlimited cell growth.

The research team compared colorectal tumor samples from patients who had taken aspirin to those who had not. Using these samples in animal studies, the researchers showed that aspirin triggers cell suicide in intestinal stem cells that carry the APC mutation, effectively killing off the cells with the potential of feeding tumor growth. Healthy intestinal cells, on the other hand, are left unscathed by aspirin.

With this important discovery of cell suicide, or programmed cell death in scientific jargon, as the instigator of aspirin’s ability to prevent colon cancer, the research team finds themselves at an exciting new starting line to find drugs for cancer patients with less harmful side effects.

As the senior author Lin Zhang states in a university press release:

“We want to use our new understanding of this mechanism as a starting point to design better drugs and effective cancer prevention strategies for those at high risk of colon cancer.”

Ideas and Energy Reveal Surprises at Stem Cell Showcase

Janssen, the company within the pharmaceutical giant Johnson & Johnson responsible for much of its research and development, has a branch in the Bay Area called J Labs. It seeks to foster innovation in all sectors of biomedical research. One piece of that effort brings together innovators for monthly gatherings to exchange ideas and network. The events have an upbeat sense of energy so it was exciting when they invited CIRM to put together an all-day session dubbed: CIRM Showcase: Accelerating Stem Cell Treatments to Patients.

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The resulting showcase yesterday had that energy. But for someone who knows the CIRM portfolio of projects backward and forward, I thought, there were a few pleasant surprises. Perhaps the most exciting news came from Linda Marban, CEO of Capricor, the company CIRM is funding to complete a clinical trial in patients with weakened hearts after a heart attack. She disclosed that the company’s next target is the heart remodeling that is the cause of death in most boys with Duchenne muscular dystrophy. She said some early data would be released at the American Heart Association meeting in Chicago in two weeks.

Another bit of news—most exciting for science wonks—came from the biotech company Sangamo that CIRM funds to develop genetically modified blood stem cells as therapy for two diseases, HIV and beta thalassemia. The firm has developed a molecular scissors called a zinc finger nuclease that can splice the DNA that makes our genes. I knew the technique was pretty precise, but Curt Herberts from the company said they had perfected it to where it could get down to a single base pair—a single link in the chain that makes up our DNA. This greatly reduces the chances for any unintended effects of the genetic manipulation.

Two advances I learned about were in using iPS type stem cells as models for disease and for discovery of traditional drugs to treat those diseases. Ashkan Javaherian, from Steve Finkbeiner’s lab at the Gladstone Institutes, described some results with the robotic microscope they have developed that lets them screen hundreds of molecules on neurons grown from iPS cells reprogrammed from patients with specific diseases. Looking just at compounds already approved by the Food and Drug Administration (FDA), ones that could be put in the clinic quickly, they found four that reduced the degradation normally seen in neurons grown from patients with Huntington’s disease.

Similarly, Joseph Wu of Stanford described his work with cells from families with various genetic heart disorders. In addition to getting individualized information from the patient-specific cells, he said they could now take it one step further and sequence the entire DNA of the cells for just $500, yielding the chance to find out exactly what mutations were causing the disease. He said it was a big step towards truly personalized medicine and to developing therapies for various racial groups that respond differently to drugs.

The day began with our President and CEO C. Randall Mills detailing his plans for a nimbler, more responsive CIRM he has dubbed CIRM 2.0. This crowd seemed thrilled with his plan for an open call for applications so that they could come in with a request when they are ready instead of forcing them into a premature application for funding because the window might not open for another year or two.

One bit of trivia drove home how difficult the entire process of moving innovative therapies into the clinic can be. Paul Laikind, CEO of ViaCyte, the company CIRM has provided more than $50 million to develop a diabetes therapy, noted the size of the application they sent to the FDA: 8,500 pages. Kind of says it all.

Don Gibbons

Bringing out the Big Guns: Scientists Weigh in on How Best to Combat Deadly Diseases of the Brain

Despite our best efforts, diseases of the brain are on the rise. Neurodegenerative conditions such as Alzheimer’s and Parkinson’s diseases threaten not only to devastate our aging population, but also cripple our economy. Meanwhile, the causes of conditions such as autism remain largely unknown. And brain and spinal cord injuries continue to increase—leaving their victims with precious few options for improving their condition.

This special review issue of addresses some of the key challenges for translational neuroscience and the path from bench to beside. [Credit: Cell Press]

This special review issue of Neuron addresses some of the key challenges for translational neuroscience and the path from bench to beside. [Credit: Cell Press]

We need to do better.

The scientific community agrees. And in a special issue of the journal Neuron, the field’s leading researchers lay out how to accelerate much-needed therapies to the many millions who will be affected by brain disease or injury in the coming years.

The journal’s leadership argues that now is the time to renew efforts in this field. Especially worrying, say experts, is the difficulty in translating research breakthroughs into therapies.

But Neuron Editor Katja Brose is optimistic that the answers are out there—we just need to bring them to light:

“There is resounding agreement that we need new approaches and strategies, and there are active efforts, discussion and experimentation aimed at making the process of therapeutic development more efficient and effective.”

Below are three papers highlighted in the special journal, each giving an honest assessment of how far we’ve come, and what we need to do to take the next step.

Fast-tracking Drug Development. In this perspective, authors from the Institute of Medicine (IOM) and the Salk Institute—including CIRM grantee Fred Gage—discuss the main takeaways from an IOM-sponsored workshop aimed at finding new avenues for accelerating treatments for brain diseases to the clinic.

The main conclusion, according to the review’s lead author Steve Hyman, is a crucial cultural shift—various stakeholders in academia, government and industry must stop thinking of themselves as competitors, but instead as allies. Only then will the field be able to successfully shepherd a breakthrough from the lab bench and to the patient’s bedside.

Downsized Divisions’ Dangerous Effects. Next, an international team of neuroscientists focuses their perspective on the recent trend of pharmaceutical companies to cut back on funding for neuroscience research. The reasoning: neurological diseases are far more difficult than other conditions, and proving to be too costly and too time-consuming to be worth continued effort.

The solution, says author Dennis Choi of State University of New York Stonybrook, is a fundamental policy change in the way that market returns of neurological disease drug development are regulated. But Choi argues that such a shift cannot be achieved without a concerted effort by patient advocates and nonprofits to lead the charge. As he explains:

“The broader neuroscience community and patient stakeholders should advocate for the crafting and implementation of these policy changes. Scientific and patient group activism has been successful in keeping the development of therapies in other areas—such as HIV and cancer—appropriately on track, but this type of sector-wide activism would be a novel step for the neuroscience community.”

Indeed, here at CIRM we have long helped support the patient community—a wonderful collection of individuals and organizations advocating for advances in stem cell research. We are humbled and honored that so many patients and patient advocates have stepped forward as stem cell champions as we move towards the clinic.

The Road to Preclinical Diagnosis. Finally, we hear from Harvard University neuroscientists highlighting how far the research has come—even in the face of such extraordinary difficulty.

Specifically focused on Alzheimer’s disease, the authors touch on the discoveries of protein markers, such as amyloid-beta and tau, that serve as an indicator of neurodegeneration. They make the important point that because Alzheimer’s is almost certainly is present before the onset of physical symptoms, the ultimate goal of researchers should be to find a way to diagnose the disease before it has progressed too far.

“[Here we] highlight the remarkable advances in our ability to detect evidence of Alzheimer’s disease in the brain, prior to clinical symptoms of the disease, and to predict those at greatest risk for cognitive decline,” explained lead author Reisa Sperling.

The common thread between these perspectives, say Neuron editors in an accompanying editorial, is that “by leveraging shared resources, tools and knowledge and approaching these difficult problems collaboratively, we can achieve more together.”

A sentiment that we at CIRM fully support—and one that we will continue to foster as we push forward with our mission to accelerate stem cell-based therapies to patients in need.

What everybody needs to know about CIRM: where has the money gone

It’s been almost ten years since the voters of California created the Stem Cell Agency when they overwhelmingly approved Proposition 71, providing us $3 billion to help fund stem cell research.

In the last ten years we have made great progress – we will have ten projects that we are funding in or approved to begin clinical trials by the end of this year, a really quite remarkable achievement – but clearly we still have a long way to go. However, it’s appropriate as we approach our tenth anniversary to take a look at how we have spent the money, and how much we have left.

Of the $3 billion Prop 71 generates around $2.75 billion was set aside to be awarded to research, build laboratories etc. The rest was earmarked for things such as staff and administration to help oversee the funding and awards.

Of the research pool here’s how the numbers break down so far:

  • $1.9B awarded
  • $1.4B spent
  • $873M not awarded

So what’s the difference between awarded and spent? Well, unlike some funding agencies when we make an award we don’t hand the researcher all the cash at once and say “let us know what you find.” Instead we set a series of targets or milestones that they have to reach and they only get the next installment of the award as they meet each milestone. The idea is to fund research that is on track to meet its goals. If it stops meetings its goals, we stop funding it.

Right now our Board has awarded $1.9B to different institutions, companies and researchers but only $1.4B of that has gone out. And of the remainder we estimate that we will get around $100M back either from cost savings as the projects progress or from programs that are cancelled because they failed to meet their goals.

So we have approximately $1B for our Board to award to new research, which means at our current rate of spending we’ll have enough money to be able to continue funding new projects until around 2020. Because these are multi-year projects we will continue funding them till around 2023 when those projects end and, theoretically at least, we run out of money.

But we are already working hard to try and ensure that the well doesn’t run dry, and that we are able to develop other sources of funding so we can continue to support this work. Without us many of these projects are at risk of dying. Having worked so hard to get these projects to the point where they are ready to move out of the laboratory and into clinical trials in people we don’t want to see them fall by the wayside for lack of support.

Of the $1.9B we have awarded, that has gone to 668 awards spread out over five different categories:

CIRM spending Oct 2014

Increasingly our focus is on moving projects out of the lab and into people, and in those categories – called ‘translational’ and ‘clinical’ – we have awarded almost $630M in funding for more than 80 active programs.

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Under our new CIRM 2.0 plan we hope to speed up the number of projects moving into clinical trials. You can read more about how we plan on doing there in this blog.

It took Jonas Salk almost 15 years to develop a vaccine for polio but those years of hard work ended up saving millions of lives. We are working hard to try and achieve similar results on dozens of different fronts, with dozens of different diseases. That’s why, in the words of our President & CEO Randy Mills, we come to work every day as if lives depend on us, because lives depend on us.