Stemson is going to use minipigs in the next stage of their hair cloning research

[Joxy]

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.

Figure 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.

Figure 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

 

[jan_miezda]

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.

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

That’s what’s useful for the things TissUse is doing by making oraganoids models. They will really speed up research on human like environment

 

[eeyore]

That’s what’s useful for the things TissUse is doing by making oraganoids models. They will really speed up research on human like environment

Too bad they've only partnered with the incapable J Hewitt so far which has done nothing with their tech over the past 3+ years.

 

[Pls_NW-1]

Great news:

A treatment for a rare genetic disease that causes cancer has become the first drug to benefit from a new fast-track approval process aimed at speeding up patients’ access to breakthrough medicines and boosting the UK’s appeal to life sciences companies post-Brexit.

The approach, which mirrors the way Britain led the world in approving the first coronavirus vaccines in December, is intended to dramatically cut the 10 years it usually takes for a new drug to move from initial concept to receiving a licence. The UK’s Medicines and Healthcare products Regulatory Agency announced on Friday that a treatment called Belzutifan has received an “innovation passport” — putting it on course to receiving a verdict in no more than 150 days after the final submission of trial data.

Cancer drug is first to begin fast-track UK approval process

Approach seeks to cut years off traditional licensing process for treatments

www.ft.com

If Stemson also falls under this category, then you could also get admission 150 days after your graduation. So with a bit of luck already in 2022/2023/2024


Geoff Hamilton, Chief Executive Officer, Stemson Therapeutics, said: “Stemson is focused on the path towards the first human trial, and to achieve this goal our focus has to be on research and development, good infrastructure, strong regulatory environment, access to scientific talent and, of course, cost.

“The UK is on our short list with its world class scientific talent and infrastructure, and I know Fortunis Capital certainly believe we will find full support for this level of scientific innovation in the UK.

“We are open to where we will eventually look at trialling it. Yes, the USA is the most valuable market – but there are clear positives in terms of research and scientific experience in the UK.


I think there is good hope. They might still have to carry out a phase two study. But I think everything should work out quickly.

Gotta kiss Stemson eg*s, if I finally can get the Norwood-1 hairline, I always wanted lol.

 

[1919]

UK to fast-track drug trials to boost post-Brexit life sciences

Companies will need to apply separately to register new medicines when Britain leaves EMA

www.ft.com

"Drugmakers will be offered fast-tracked approvals for innovative medicines in the UK as ministers seek to build on the country’s world-leading approval of a Covid vaccine and attract life sciences companies to invest post-Brexit".

I hope that goes quickly

Drug trials to be fast-tracked after Brexit as ministers relax rules

New laws will be designed to create a ‘streamlined, internationally competitive’ process to ensure that patients get the latest treatments

www.independent.co.uk

"Ministers plan to fast-track new drugs after Brexit​

New laws will be designed to create a ‘streamlined, internationally competitive’ process to ensure that patients get the latest treatments"​

What is the probability that a cosmetic procedure gets approved? Plus, correct me if im wrong, but this would be the first commercialized procedure involving the implantation of a cloned organ onto the human body in all of history. Fast-tracking something so unknown seems a bit of a stretch.
Nevertheless, medical treatments are getting approved faster which is exceptional news.
p.s. sorry hate to be that guy. Someone has to tame our hopes right??

 

[1919]

[https://www.nice.org.uk/news/articl...ocess-for-new-medicines-opened-on-january-1st]

“Now we have left the EU, we have the freedom to innovate and cut red tape to speed up the approval process for new treatments and ensure patient safety is at the heart of everything we do.

“The new pathway represents a totally new way of thinking and is a truly collaborative approach between the healthcare system, the pharmaceutical industry and patients with the common goal of getting the best products to the people who need them as safely and quickly as possible.”

From:

Innovative Licensing and Access Pathway

A new pathway supporting innovative approaches to the safe, timely and efficient development of medicines to improve patient access.

www.gov.uk

Seems to be a bureaucratic change that allows companies to collaborate with regulatory entities faster. This is implication that the process initially took 10 years due to system inefficiencies rather than due to regulations. So my allusion that fast-tracking would not be possible due to safety regulations does not apply to the same extent. Although, it would be interesting to discuss whether cloned hair requires long-term studies. For a skin deep procedure, is potential harm a concern?
Anyways, YAY! Stemson could very well benefit from this system. Thanks for the news NoMoney.
Guys, lets take a moment to realize the implications of cloning an organ and implanting it. Its absolutely INSANE! would be the mark of a true anti-aging era. In the next few decades, how long will humans be able to live? will organ failure be a thing of the past? But more importantly, will I still have my hair??
EDIT: I misinterpreted the criteria list. Stemson would very unlikely be eligible. Thanks to Yadonkey.

 

[trialAcc]

[https://www.nice.org.uk/news/articl...ocess-for-new-medicines-opened-on-january-1st]

“Now we have left the EU, we have the freedom to innovate and cut red tape to speed up the approval process for new treatments and ensure patient safety is at the heart of everything we do.

“The new pathway represents a totally new way of thinking and is a truly collaborative approach between the healthcare system, the pharmaceutical industry and patients with the common goal of getting the best products to the people who need them as safely and quickly as possible.”

From:

Innovative Licensing and Access Pathway

A new pathway supporting innovative approaches to the safe, timely and efficient development of medicines to improve patient access.

www.gov.uk

Seems to be a bureaucratic change that allows companies to collaborate with regulatory entities faster. This is implication that the process initially took 10 years due to system inefficiencies rather than due to regulations. So my allusion that fast-tracking would not be possible due to safety regulations does not apply to the same extent. Although, it would be interesting to discuss whether cloned hair requires long-term studies. For a skin deep procedure, is potential harm a concern?
Anyways, YAY! Stemson could very well benefit from this system. Thanks for the news NoMoney.
Guys, lets take a moment to realize the implications of cloning and implanting an organ. Its absolutely INSANE! would be the mark of a true anti-aging era. In the next few decades, how long will humans be able to live? will organ failure be a thing of the past?

Fast tracking exists in the USA with the FDA as well, it still takes 5+ years. It just allows companies to initiate phase 1/2 trails and 2/3 trials instead of 1 => 2 => 3 => Review filing => approval, while also testing on fewer people then normally required. In certain (serious) cases like cancers & fatal orphan diseases you can even get the product to people after the phase 1/2 is completed and have a phase 3 review study be pending for up to 5 years.

 

[1919]

Fast tracking exists in the USA with the FDA as well, it still takes 5+ years. It just allows companies to initiate phase 1/2 trails and 2/3 trials instead of 1 => 2 => 3 => Review filing => approval. In certain (serious) cases like cancers & fatal orphan diseases you can even get the product to people after the phase 1/2 is completed and have a phase 3 review study be pending for up to 5 years.

The consensus here is that the FDA is slow with cosmetic procedures which is completely understandable. ILAP seems to be a fast-track that has an emphasis on innovation relative to the FDA (im assuming, please correct me if I am wrong) like NoMoney says. If haircloning is considered ATMP it could be fast-tracked even if its not a cure to a "life-threatening" disease.
I still think that haircloning will require more than 5 years of trialling before approval even with all the fast-tracking. The reasons for this is because 1) I assume cloning has a ton of unknown mechanisms. So long term safety especially in regards to cancer is significant. 2) Hair takes a while to grow (how do we know how long the cloned grafts will last)?
What do you think trialAcc? I don't have a scientific background on hair cloning, so I'm not in a place to give any valid estimates.
EDIT: I misinterpreted the criteria list. Stemson would very unlikely be eligible. Thanks to Yadonkey.

 

[eeyore]

I feel like Stemson doesn't really have the funding to do anything in the UK, and if they did make the move it'd probably cause more delays.

 

[trialAcc]

I feel like Stemson doesn't really have the funding to do anything in the UK, and if they did make the move it'd probably cause more delays.

I think they specifically got Fotunis Capital involved because of the UK move.

The consensus here is that the FDA is slow with cosmetic procedures which is completely understandable. ILAP seems to be a fast-track that has an emphasis on innovation relative to the FDA (im assuming, please correct me if I am wrong) like NoMoney says. If haircloning is considered ATMP it could be fast-tracked even if its not a cure to a "life-threatening" disease.
I still think that haircloning will require more than 5 years of trialling before approval even with all the fast-tracking. The reasons for this is because 1) I assume cloning has a ton of unknown mechanisms. So long term safety especially in regards to cancer is significant. 2) Hair takes a while to grow (how do we know how long the cloned grafts will last)?
What do you think trialAcc? I don't have a scientific background on hair cloning, so I'm not in a place to give any valid estimates.

Well first, I don't have a science background either, but to the point, I don't think the process will be any longer/shorter then with any other clinical trials because it's cloning (in fact if it was a localized procedure it'd probably be quicker). The safety aspect would be looking at how the body reacted to the implantation/procedure similar to how the body is monitored after a organ transplant. If the body were to have an acute immune reaction or reject the follicles it would probably happen within the first life-cycle of the follicle. The length of the life of the follicle probably won't be something they look for in the trials. I'm assuming it would just be the functional characteristics and health of it compared to a native one.

Either way, this is all sort of baseless speculation right now because we don't seem to know a lot of about the procedure. If they were implanting cultured follicles into the head like Riken/a hair transplant, the regulatory hurdle will be a lot more minimal than if the follicles were actually being dosed/created within your scalp.

 

[eeyore]

I think they specifically got Fotunis Capital involved because of the UK move.

Well first, I don't have a science background either, but to the point, I don't think the process will be any longer/shorter then with any other clinical trials because it's cloning (in fact if it was a localized procedure it'd probably be quicker). The safety aspect would be looking at how the body reacted to the implantation/procedure similar to how the body is monitored after a organ transplant. If the body were to have an acute immune reaction or reject the follicles it would probably happen within the first life-cycle of the follicle. The length of the life of the follicle probably won't be something they look for in the trials. I'm assuming it would just be the functional characteristics and health of it compared to a native one.

Either way, this is all sort of baseless speculation right now because we don't seem to know a lot of about the procedure. If they were implanting cultured follicles into the head like Riken/a hair transplant, the regulatory hurdle will be a lot more minimal than if the follicles were actually being dosed/created within your scalp.

I'm not nearly as informed in this field as you, but I would've thought Stemson took whatever money they could. Also, Fortunis is pretty new and poor for a VC from what I've seen, I don't think they have the resources to spare to get Stemson to the UK.

 

[trialAcc]

I'm not nearly as informed in this field as you, but I would've thought Stemson took whatever money they could. Also, Fortunis is pretty new and poor for a VC from what I've seen, I don't think they have the resources to spare to get Stemson to the UK.

I don't think it's nearly as expensive or jarring to do registered trials in a different country as you seem to imply. Several millions of dollars in funding would be enough, which Fortunis should certainly be able to inject.

 

[1919]

I think they specifically got Fotunis Capital involved because of the UK move.

Well first, I don't have a science background either, but to the point, I don't think the process will be any longer/shorter then with any other clinical trials because it's cloning (in fact if it was a localized procedure it'd probably be quicker). The safety aspect would be looking at how the body reacted to the implantation/procedure similar to how the body is monitored after a organ transplant. If the body were to have an acute immune reaction or reject the follicles it would probably happen within the first life-cycle of the follicle. The length of the life of the follicle probably won't be something they look for in the trials. I'm assuming it would just be the functional characteristics and health of it compared to a native one.

Either way, this is all sort of baseless speculation right now because we don't seem to know a lot of about the procedure. If they were implanting cultured follicles into the head like Riken/a hair transplant, the regulatory hurdle will be a lot more minimal than if the follicles were actually being dosed/created within your scalp.

Great insight. I think you are closer to the truth than I am.

 

[1919]

if stemson offers a cure for under 15k in the next 5 years, i will name my son stemson.

and Tsuji, if Tsuji succeeds. Or Hairlosstalk in honor of this website.

 

[MrV88]

Would laugh my *** off if Stemson would be available sooner than Tsuji, that face would be hilarious, but still the beginning of clinical trials, funding, delays, pandemics and 817391 other possibilities tell me to wait another 5 years.

 

[trialAcc]

Would laugh my *** off if Stemson would be available sooner than Tsuji, that face would be hilarious, but still the beginning of clinical trials, funding, delays, pandemics and 817391 other possibilities tell me to wait another 5 years.

I think this is easily the safe bet. One is VC funded and has business development plans, the other is asking for donations on Twitter.

 

[Pls_NW-1]

I think this is easily the safe bet. One is VC funded and has business development plans, the other is asking for donations on Twitter.

and re-tweeting political posts wtf

 

[pegasus2]

if stemson offers a cure for under 15k in the next 5 years, i will name my son stemson.

At least you won't have to name your son Stemson.

 

[1919]

Stemson wouldn't qualify for an innivation passport, its pretty clear. They have to fill the criteria, they fall at the first hurdle.

a) the condition is life-threatening or seriously debilitating or

b) there is a significant patient or public health need

Hair loss is not life threatening or seriously debilitating and despite what users on here think, there isn't a significant need for it within the public health sector.

Oh I must have misinterpreted the criteria. So stemson must fall in all 1, 2, and 3 criteria in order to be approved. Sorry if I confused anyone.

 

[1919]

"You will then be invited to meet with the MHRA to discuss how your product fulfils the three criteria."

They might try, who knows - the government may be welling to bend slightly and and give them an innovation passport for ILAP if it's beneficial to them.


But if you're following the actual criteria, it seems that they wouldn't qualify.

Ya. Then again, hairloss treatment would be pretty absurd to fast-track. As a matter of fact, any cosmetic treatment. It is much better to prioritize life-threatening/ debilitating conditions even if I do hope stemson gets some bureaucratic support somewhere.