Yeah I don't usually go past midnight lol but I also get paid less.
Stemson is going to use minipigs in the next stage of their hair cloning research
- Thread starter werefckd
- Start date
One thing that I found very important in that small presentation was that Fortunis plans to exit prior to commercialization and allow "the Abbvie's of the world" bring the product to market. Unlike whatever Tsuji is doing, this is the proper way to structure the development of this type of product. Hopefully they have that structured out well in advance so it doesn't cause delays.
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I've heard that their goal is 2027... and now expect some delays... 2030 min. for this.
Maybe even 2035 for a realist. Lol
This means they know they don't have the money to help Stemson commercialize right?
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stop repeating that in 15-30 years it will be launched, etc. If you thought so, it wouldn't be like it is now, literally all the time online in this forum. you carry 900 messages in a month, I know your problem is different from the rest but do yourself a favor and go out for a while and relax.
That's unfortunate, if anything I'd hope at least the success in pigs part is true since if it is, it'd most likely be just a matter of time and money.
No, without doing any research at all it probably just means they see their value proposition as being centered around early stage investments rather then late stage. They invest the seed or series A financing (usually low to mid 8 figures) and then when the value of the company is more defined and several multiples higher they sell their stake.
Basically they are the money men, not the strategic partner and they know this. When it comes to biotech this is probably a good thing. Do you want a group of rich guys overseeing this or one of the biggest biotech companies in the world?
He's not just pulling things out of his ***, though. They are talking about turning blank cells into hair follicles. Clearly if that were successful at that they would be able to regenerate unlimited follicles.
What I found more interesting was that he said "without transplantation". I thought this was going to be a similar procedure to a transplant but it sounds like its an injection or prp type procedure now?
But wouldn't it make more sense to keep their stake through commercialization since that's when the money comes?
I think by "without transplantation" he only means that hairs don't have to be taken from the donor area. From everything we know, it will be an implantation of cloned hair follicles similar to how follicles are inserted in a traditional hair transplant operation, and not an injection, though perhaps much less invasive.
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Could be, but that might not be the investment style of the VC firm. They might prefer quicker exits and just flipping the ownership share while the company value is still estimated rather then realized but has still significant increased.
You also need to consider that the product can still make it to market and fail financially or just flat out fail to be safe. A competitor could come to market with a better solution, the market usage could be less then predicted because the process is invasive, etc.
How significant do you think it is that Stemson is already in the talks or has partnerships with surgeons representing the doctors who would potentially carry out the treatment?
I feel like it is a good sign that they're confident and that third parties have confidence in them as they're already beginning to build an infrastructure for for commercialization, but I have no idea as to the actual significance of it or whether it's just for show to increase the value of their company.
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this is just a little anecdote from personal experience, but for what it's worth: i was examined by so-cal doctor specializing in hair restoration last year, guy who far as i can tell is highly respected... i asked during our consultation about future treatments, and he alluded to stemson, said he's partnered to some degree and is excited about their future... in terms of timeline, he gave me the ole "5 years," which no one likes to hear at this point... i'll probably have to see him again at some point, i will ask again, who knows, being a so-cal guy (and not being short on money tbh), maybe i even get some early sneak peak or even participation in stemson, but of course i don't want to get ahead of myself, for all i know stemson is doomed to fail, but i sure hope it's just the opposite
Stemson's CEO has stated it near the end of the video here:
That's somewhat encouraging news, thanks for sharing.
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no problem, it's not much, i assume other people here have stories like that from their consultations, maybe i'm in unique position being in los angeles, idk... i'm still in my 20s until the very end of 2024, certainly not crossing my fingers that these innovations will be available by then, but it's not totally inconceivable... i'd just like to get a legit positive update from this guy at some consultation in the next few years, i guess that's good enough
I think we're more or less the same age though I haven't gone in for any consultation yet. I'm waiting for more definitive news on a cure before I expend my donor supply on my hairline.
The fact that the surgeon you went to told you about Stemson and gave you a timeline of "in five years" may imply that he's optimistic about Stemson as, unless I may have missed something, he's essentially telling you to hold off on a transplant for now? Either that or your hair is still holding up well for now and he gave you responsible advice.
For what it's worth, I highly doubt the timeline of 2025 for Stemson to commercialize but I am somewhat confident in their team and method and have a (in my opinion) fairly reasonable expectation for a widely available cure (for those who are willing to spend at least $100k on it) some time around 2030 assuming things don't go horribly.
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yeah he advised to hold off, i wasn't even going in expecting to book a transplant i guess, just wanted more info
Why Drugs Tested in Mice Fail in Human Clinical Trials
by Sam Zimmerman
figures by Hannah Zucker
If we were all mice, Alzheimer’s disease, cancer, diabetes, and most inherited disorders would be a thing of the past. We could nibble on as much cheese as we wanted without fear of heart disease and run around our favorite wheel for hours on end without knee pain because all these ailments have been cured in mice. Unfortunately, we are not mice, and most of these cures fail miserably in humans. Out of the hundreds of Alzheimer’s disease treatments that helped mice, none have been beneficial to people. But why do Alzheimer’s treatments that show so much promise in animals never work on human beings? Even though mice and humans look slightly different from each other, they share 92% of their DNA. Additionally, humans and mice have identical genes. One would think a drug that targets and activates a gene in mice would also activate the gene in humans, but this is not always true.
The same gene in mice and humans are used in different ways
A recent study published in Nature by Hodge et al. showed that even though humans and mice share the same genes, they function differently in the cells of different animals. In order for a cell to perform its job properly, it needs to make specific proteins unique to that cell. These proteins are the worker bees, the ones that actually do the job of a cell, and the directions used to make these proteins are encoded in sections of DNA called genes. A gene is like a very important sentence of a book that a cell can read every time it wants to make the protein encoded by the gene. The more the cell reads the gene, the more the gene is expressed, and the more protein that is made. All of the 20,000 genes in the human genome can be read an infinite number of times, allowing a cell to make many different types of proteins particular to its needs.To compare genes in humans and mice, Hodge et al. used a technique called DNA sequencing to identify the DNA that makes up all the genes in human and mouse brain cells. The researchers learned that almost every type of cell in the mouse brain, including almost all neurons, is also present in the human brain. However, once researchers compared the expression of individual genes within the same cell type, they found vast differences between mice and humans. Two-thirds of all genes shared between mice and humans are expressed differently in the same cell type. The most striking difference was found in neurons, where several genes used to make serotonin receptors are turned on in mice but off in humans. Serotonin, a chemical that regulates mood, sends messages between neurons by binding to its receptor on the receiving neuron’s surface. Without the receptor, serotonin cannot transmit signals to nearby cells. If drugs are made to target receptors that are only present in mice, they will not work in humans. As a result, treatments for depression, schizophrenia, anxiety, Alzheimer’s, and other disorders may be very helpful in mice but would fail to treat the diseases in humans.
Even though genes in mice and human brains are quite different, some parts of the body in humans and mice are more alike. When researchers from the Broad Institute of Harvard and MIT compared the expression of genes in human and mice immune systems, only 169 genes were turned on in one species but off in the other, a much smaller number than the 9,000 genes on in one species but off in the other in the brain. However, a change to a single gene can be the difference between success and failure in clinical trials. This illustrates that, while mice may model the immune system of humans better than the brain, studies that show drug efficacy in immune disorders should still be treated with caution.
When differences between human and mice prove fatal
Sometimes these seemingly small differences between humans and mice can have disastrous consequences. Just like a dog cannot eat chocolate because their liver cannot break down the caffeine, humans have also died because their bodies cannot absorb or process the drugs originally tested in mice. In 1993 the drug fialuridine (FIAU) was developed to treat people with hepatitis B and worked amazingly well in mice, rats, dogs, and primates, but once human trials were underway seven people developed liver failure and five died. FIAU was toxic in humans because of a specific protein located on our mitochondria, the structures that generate energy in our cells. This protein transports the drug from empty space in the cell into the mitochondria. Once the drug is let in, it poisons the mitochondria. This turns off the energy supply to our livers where the drug is absorbed. Even though this protein is also present in mice, it does not send the drug into mitochondria because of only 3 differences in the DNA of mice. These 3 DNA mutations change the gene encoding the protein just enough to keep it away from the cell’s mitochondria so the protein cannot transfer the drug into it.Research methods may also cause drug trials to fail
Clearly, mice are not the perfect model of every human disease, but scientists still use them to study most ailments out of convenience. To fully replicate complex diseases in mice, researchers would have to know exactly which genes are mutated in humans and make these same mutations to a mouse’s genome. Unfortunately, this knowledge is not usually available. Instead, researchers mutate a small number of genes to replicate the symptoms of a disease. In reality, these mice rarely have all the symptoms of a disease, such as the shaking seen in Huntington’s disease. Additionally, complex diseases such as Alzheimer’s involve many different changes in human genes, and it is unlikely that mice with only some of the changes will have the same underlying illness as humans. So even if a mouse is cured of its illness, that is no guarantee it will cure the human disease the researchers attempt to copy in the mice.Researchers are devoted to making every experiment reproducible so other people can check their work. Normally this is a good thing, but to do this in experiments with mice, researchers use mice that, through breeding, have exactly the same DNA. That way, other researchers can use the same mice and get the same result. Curing mice with identical DNA is like devising a cure for only one human out of the 7.5 billion people on Earth. Every person responds differently to medicine and illnesses; what works in one person may not work in another person with different DNA. Some researchers have encouraged scientists to accept that variation in experiments is inevitable. Instead of relying on a single type of mouse with specific DNA, researchers should design experiments that account for this natural variation.
Ironically, even when researchers use the same strains of mice, poor study design and differing methodologies can prevent experiments from being reproducible. In a systematic review of the stroke treatment nimodipine on mice, researchers found the methodologies used in the experiments were poor and there was no consensus on the nimodipine’s effect on stroke. Only 50% of the studies found nimodipine helped relieve symptoms, while the others found no benefit from the drug.
Alternatives to the mouse model
In many ways, mice are ideal for scientific experiments. They are genetically similar to humans, produce many offspring, and mature quickly so that experiments can be done in a short time period. They have helped to develop treatments for numerous diseases, from diabetes to cancer. In 2011, sickle cell disease, a disorder that prevents red blood cells from delivering oxygen to the rest of the body, was cured in mice by decreasing the expression of one gene, allowing for new, healthy red blood cells to form. Just last year, the same strategy was used to create a novel gene therapy that has successfully treated humans as well.However, in complex neurological disorders where many genes are disrupted, mice are unlikely to model the disease correctly, making a cure for humans less likely. In these cases, some researchers suggest studying human cells in isolation and abandoning mice models. Another alternative to performing research on mice is to use animals such as primates that are more similar to humans. However, as seen in the FIAU example, treatments that work in primates are not guaranteed to work in humans. Ultimately, there is no one-size-fits-all solution, and the best answer may not lie in the type of animal we use at all. Instead, improvements in scientific methods and systematic reviews of animal research that inform the design of clinical trials may be the best way to improve a drug’s success rate.
Sam Zimmerman is a Ph.D. student in the Biological and Biomedical Sciences program at Harvard University.
Hannah Zucker is a Ph.D. student in the Program in Neuroscience at Harvard University.
Cover image: “Apodemus sylvaticus bosmuis” by Rasbak is licensed under CC BY-SA 3.0
Why Drugs Tested in Mice Fail in Human Clinical Trials - Science in the News
Mice are considered a standard method for drug development in humans, but are these species an ideal model of the human brain?
sitn.hms.harvard.edu
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- 292
That’s what’s useful for the things TissUse is doing by making oraganoids models. They will really speed up research on human like environmentWhy Drugs Tested in Mice Fail in Human Clinical Trials
by Sam Zimmerman
figures by Hannah Zucker
If we were all mice, Alzheimer’s disease, cancer, diabetes, and most inherited disorders would be a thing of the past. We could nibble on as much cheese as we wanted without fear of heart disease and run around our favorite wheel for hours on end without knee pain because all these ailments have been cured in mice. Unfortunately, we are not mice, and most of these cures fail miserably in humans. Out of the hundreds of Alzheimer’s disease treatments that helped mice, none have been beneficial to people. But why do Alzheimer’s treatments that show so much promise in animals never work on human beings? Even though mice and humans look slightly different from each other, they share 92% of their DNA. Additionally, humans and mice have identical genes. One would think a drug that targets and activates a gene in mice would also activate the gene in humans, but this is not always true.
The same gene in mice and humans are used in different ways
A recent study published in Nature by Hodge et al. showed that even though humans and mice share the same genes, they function differently in the cells of different animals. In order for a cell to perform its job properly, it needs to make specific proteins unique to that cell. These proteins are the worker bees, the ones that actually do the job of a cell, and the directions used to make these proteins are encoded in sections of DNA called genes. A gene is like a very important sentence of a book that a cell can read every time it wants to make the protein encoded by the gene. The more the cell reads the gene, the more the gene is expressed, and the more protein that is made. All of the 20,000 genes in the human genome can be read an infinite number of times, allowing a cell to make many different types of proteins particular to its needs.
View attachment 157461Figure 1. Two cells with the same set of genes can express different proteins by regulating how DNA is “read” into protein, as shown in panel A. In the example shown in B, the neuron on the left panel expresses the gene for a serotonin receptor, whereas the neuron in the right panel has the same gene but does not express the serotonin receptor. Consequently, a drug designed to act on the serotonin receptor will affect the left neuron on the left but not the one on the right.
To compare genes in humans and mice, Hodge et al. used a technique called DNA sequencing to identify the DNA that makes up all the genes in human and mouse brain cells. The researchers learned that almost every type of cell in the mouse brain, including almost all neurons, is also present in the human brain. However, once researchers compared the expression of individual genes within the same cell type, they found vast differences between mice and humans. Two-thirds of all genes shared between mice and humans are expressed differently in the same cell type. The most striking difference was found in neurons, where several genes used to make serotonin receptors are turned on in mice but off in humans. Serotonin, a chemical that regulates mood, sends messages between neurons by binding to its receptor on the receiving neuron’s surface. Without the receptor, serotonin cannot transmit signals to nearby cells. If drugs are made to target receptors that are only present in mice, they will not work in humans. As a result, treatments for depression, schizophrenia, anxiety, Alzheimer’s, and other disorders may be very helpful in mice but would fail to treat the diseases in humans.
Even though genes in mice and human brains are quite different, some parts of the body in humans and mice are more alike. When researchers from the Broad Institute of Harvard and MIT compared the expression of genes in human and mice immune systems, only 169 genes were turned on in one species but off in the other, a much smaller number than the 9,000 genes on in one species but off in the other in the brain. However, a change to a single gene can be the difference between success and failure in clinical trials. This illustrates that, while mice may model the immune system of humans better than the brain, studies that show drug efficacy in immune disorders should still be treated with caution.
When differences between human and mice prove fatal
Sometimes these seemingly small differences between humans and mice can have disastrous consequences. Just like a dog cannot eat chocolate because their liver cannot break down the caffeine, humans have also died because their bodies cannot absorb or process the drugs originally tested in mice. In 1993 the drug fialuridine (FIAU) was developed to treat people with hepatitis B and worked amazingly well in mice, rats, dogs, and primates, but once human trials were underway seven people developed liver failure and five died. FIAU was toxic in humans because of a specific protein located on our mitochondria, the structures that generate energy in our cells. This protein transports the drug from empty space in the cell into the mitochondria. Once the drug is let in, it poisons the mitochondria. This turns off the energy supply to our livers where the drug is absorbed. Even though this protein is also present in mice, it does not send the drug into mitochondria because of only 3 differences in the DNA of mice. These 3 DNA mutations change the gene encoding the protein just enough to keep it away from the cell’s mitochondria so the protein cannot transfer the drug into it.
View attachment 157462Figure 2. Fialuridine (FIAU) is toxic to humans but not mice because of a difference in protein localization. In both mice and humans, FIAU enters the cell through a transporter protein in the cell membrane and acts against Hepatitis B Virus (HBV). In humans, the transporter protein is also located on the mitochondrial membrane, so FIAU enters the mitochondria and poisons this important energy-generating part of the cell. The mouse transporter is not located on the mitochondria, so FIAU cannot enter the mitochondria and exert its toxic effect.
Research methods may also cause drug trials to fail
Clearly, mice are not the perfect model of every human disease, but scientists still use them to study most ailments out of convenience. To fully replicate complex diseases in mice, researchers would have to know exactly which genes are mutated in humans and make these same mutations to a mouse’s genome. Unfortunately, this knowledge is not usually available. Instead, researchers mutate a small number of genes to replicate the symptoms of a disease. In reality, these mice rarely have all the symptoms of a disease, such as the shaking seen in Huntington’s disease. Additionally, complex diseases such as Alzheimer’s involve many different changes in human genes, and it is unlikely that mice with only some of the changes will have the same underlying illness as humans. So even if a mouse is cured of its illness, that is no guarantee it will cure the human disease the researchers attempt to copy in the mice.
Researchers are devoted to making every experiment reproducible so other people can check their work. Normally this is a good thing, but to do this in experiments with mice, researchers use mice that, through breeding, have exactly the same DNA. That way, other researchers can use the same mice and get the same result. Curing mice with identical DNA is like devising a cure for only one human out of the 7.5 billion people on Earth. Every person responds differently to medicine and illnesses; what works in one person may not work in another person with different DNA. Some researchers have encouraged scientists to accept that variation in experiments is inevitable. Instead of relying on a single type of mouse with specific DNA, researchers should design experiments that account for this natural variation.
Ironically, even when researchers use the same strains of mice, poor study design and differing methodologies can prevent experiments from being reproducible. In a systematic review of the stroke treatment nimodipine on mice, researchers found the methodologies used in the experiments were poor and there was no consensus on the nimodipine’s effect on stroke. Only 50% of the studies found nimodipine helped relieve symptoms, while the others found no benefit from the drug.
Alternatives to the mouse model
In many ways, mice are ideal for scientific experiments. They are genetically similar to humans, produce many offspring, and mature quickly so that experiments can be done in a short time period. They have helped to develop treatments for numerous diseases, from diabetes to cancer. In 2011, sickle cell disease, a disorder that prevents red blood cells from delivering oxygen to the rest of the body, was cured in mice by decreasing the expression of one gene, allowing for new, healthy red blood cells to form. Just last year, the same strategy was used to create a novel gene therapy that has successfully treated humans as well.
However, in complex neurological disorders where many genes are disrupted, mice are unlikely to model the disease correctly, making a cure for humans less likely. In these cases, some researchers suggest studying human cells in isolation and abandoning mice models. Another alternative to performing research on mice is to use animals such as primates that are more similar to humans. However, as seen in the FIAU example, treatments that work in primates are not guaranteed to work in humans. Ultimately, there is no one-size-fits-all solution, and the best answer may not lie in the type of animal we use at all. Instead, improvements in scientific methods and systematic reviews of animal research that inform the design of clinical trials may be the best way to improve a drug’s success rate.
Sam Zimmerman is a Ph.D. student in the Biological and Biomedical Sciences program at Harvard University.
Hannah Zucker is a Ph.D. student in the Program in Neuroscience at Harvard University.
Cover image: “Apodemus sylvaticus bosmuis” by Rasbak is licensed under CC BY-SA 3.0
Why Drugs Tested in Mice Fail in Human Clinical Trials - Science in the News
Mice are considered a standard method for drug development in humans, but are these species an ideal model of the human brain?sitn.hms.harvard.edu