I had no idea, wow. It always surprises me how quiet these companies make their failures, not that I expect a big press conference -- and then they expunge all evidence of the failed drug's existence from the record to pretend it never even happened.
I also looked at the other Merck phase II drug, c-6443, and it looks to me like that might have been the same drug with a name change, because there is also no record of it on Merck's website after 2003. So I'll delete that one as well.
Summary of the pipeline
Based on the information below, I put PI-2301 in pre-clinical. It looks like they're hoping to start phase I trials in the next few months.
It is known that random sequence peptides composed of certain amino acids are able to affect the activity of the CD4+ T-cells involved in the development and progression of multiple sclerosis. PI-2301 represents a new generation of random sequence peptides that are expected to have superior efficacy and convenience profiles compared to current immunomodulating agents for the treatment of multiple sclerosis. Peptimmune's random sequence peptide PI-2301 is a mixture of polypeptides synthesized in a random sequence of four different amino acids. It is different in composition than Copaxone®, a random copolymer of the amino acids glutamic acid, tyrosine, alanine and lysine, which has been approved as immunomodulatory therapy for MS. Peptimmune's founders discovered that substitution of one of the four amino acids that comprise Copaxone led to better binding of the peptide with the MHC Class II complex on the surface of antigen presenting cells and T-cells.
Preclinical Development
Pre-clinical studies have shown that PI-2301 has a greater binding affinity for MHC binding domain from MS patients than does Copaxone. The new peptides have been found to be more effective than Copaxone® in in-vitro and in-vivo assays, as well as in animal disease models of MS.
Clinical Development
Peptimmune is currently completing pre-clinical development and IND enabling toxicology studies with PI-2301. Phase I clinical trials are expected to begin in 2006.
http://www.peptimmune.com/co14.asp
It is known that random sequence peptides composed of certain amino acids are able to affect the activity of the CD4+ T-cells involved in the development and progression of multiple sclerosis. PI-2301 represents a new generation of random sequence peptides that are expected to have superior efficacy and convenience profiles compared to current immunomodulating agents for the treatment of multiple sclerosis. Peptimmune's random sequence peptide PI-2301 is a mixture of polypeptides synthesized in a random sequence of four different amino acids. It is different in composition than Copaxone®, a random copolymer of the amino acids glutamic acid, tyrosine, alanine and lysine, which has been approved as immunomodulatory therapy for MS. Peptimmune's founders discovered that substitution of one of the four amino acids that comprise Copaxone led to better binding of the peptide with the MHC Class II complex on the surface of antigen presenting cells and T-cells.
Preclinical Development
Pre-clinical studies have shown that PI-2301 has a greater binding affinity for MHC binding domain from MS patients than does Copaxone. The new peptides have been found to be more effective than Copaxone® in in-vitro and in-vivo assays, as well as in animal disease models of MS.
Clinical Development
Peptimmune is currently completing pre-clinical development and IND enabling toxicology studies with PI-2301. Phase I clinical trials are expected to begin in 2006.
http://www.peptimmune.com/co14.asp
Another one for pre-clinical: fasudil.
The selective Rho-kinase inhibitor Fasudil is protective and therapeutic in experimental autoimmune encephalomyelitis.
J Neuroimmunol. 2006 Sep 20;
Sun X, Minohara M, Kikuchi H, Ishizu T, Tanaka M, Piao H, Osoegawa M,
Ohyagi Y, Shimokawa H, Kira JI.
Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
We studied the role of fasudil, a selective Rho-kinase inhibitor, in experimental autoimmune encephalomyelitis (EAE). Both parenteral and oral administration of fasudil prevented the development of EAE induced by proteolipid protein (PLP) p139-151 in SJL/J mice. Specific proliferation of lymphocytes to PLP was significantly reduced, together with a downregulation of interleukin (IL)-17 and a marked decrease of the IFN-gamma/IL-4 ratio. Immunohistochemical examination also disclosed a marked decrease of inflammatory cell infiltration, and attenuated demyelination and acute axonal transaction.
These results may provide a rationale of selective blockade of Rho-kinase by oral use of fasudil as a new therapy for multiple sclerosis.
<shortened url>
The selective Rho-kinase inhibitor Fasudil is protective and therapeutic in experimental autoimmune encephalomyelitis.
J Neuroimmunol. 2006 Sep 20;
Sun X, Minohara M, Kikuchi H, Ishizu T, Tanaka M, Piao H, Osoegawa M,
Ohyagi Y, Shimokawa H, Kira JI.
Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
We studied the role of fasudil, a selective Rho-kinase inhibitor, in experimental autoimmune encephalomyelitis (EAE). Both parenteral and oral administration of fasudil prevented the development of EAE induced by proteolipid protein (PLP) p139-151 in SJL/J mice. Specific proliferation of lymphocytes to PLP was significantly reduced, together with a downregulation of interleukin (IL)-17 and a marked decrease of the IFN-gamma/IL-4 ratio. Immunohistochemical examination also disclosed a marked decrease of inflammatory cell infiltration, and attenuated demyelination and acute axonal transaction.
These results may provide a rationale of selective blockade of Rho-kinase by oral use of fasudil as a new therapy for multiple sclerosis.
<shortened url>
Based on this, I'll move CDP 323 from phase I to phase II.
CDP 323 in multiple sclerosis - Phase II study expected to start in Q1 2007
UCB provides a top line update on the clinical programme evaluating CDP 323 in healthy volunteers. CDP 323 is a potent and orally active small molecule antagonist of alpha 4-integrin. A phase I trial in human volunteers was successfully completed allowing UCB to progress to a phase II study in Multiple Sclerosis in Q1 2007. The results of phase I studies will be presented at the 2006 European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) meeting to be held in Madrid on 27 September 2006.
http://www.marketwire.com/mw/release_ht ... _id=166649
CDP 323 in multiple sclerosis - Phase II study expected to start in Q1 2007
UCB provides a top line update on the clinical programme evaluating CDP 323 in healthy volunteers. CDP 323 is a potent and orally active small molecule antagonist of alpha 4-integrin. A phase I trial in human volunteers was successfully completed allowing UCB to progress to a phase II study in Multiple Sclerosis in Q1 2007. The results of phase I studies will be presented at the 2006 European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) meeting to be held in Madrid on 27 September 2006.
http://www.marketwire.com/mw/release_ht ... _id=166649
First the bad news: I was looking on the Eisai website, then on Clinicaltrials.gov and couldn't find any sign of the former phase II study of E2007, so I'm deleting it. Let me know if this is a mistake.
On the bright side, I had EPO in the pre-clinical stage, but it looks like EPO has already had some phase II trials and is likely to have a phase IIb trial coming up soon, based on the information below (sorry if somebody already posted this and I missed it):
Stem Cell Therapeutics Corp. (SCT), a Canadian biotechnology company engaged in treating central nervous system (CNS) disorders by stimulating endogenous neural stem cells, is pleased to announce that it has entered into an Option to Acquire agreement for up to two additional clinical stage programs, one in schizophrenia and the other in multiple sclerosis. The agreement between SCT and two researchers from the Max
Planck Institute of Experimental Medicine in Germany provides SCT with the right, but not the obligation, to acquire one or both of the clinical stage
programs under option.
The two programs optioned under the agreement also employ EPO as a therapeutic intervention for severe, poorly treated neurological conditions, in this case schizophrenia and multiple sclerosis. If the Option to Acquire is exercised by SCT, the company will have three Phase II clinical programs in progress that employ EPO alone or in combination with other agents for the treatment of serious CNS diseases.
The multiple sclerosis program captured in the agreement has already completed a 24 week open label Phase IIa clinical study seeking improvement in walking distance and Kurtzke Expanded Disability Status Scale (EDSS) efficacy endpoints in chronic progressive multiple sclerosis patients treated with high vs. low doses of EPO. The next clinical development step for the multiple sclerosis program is likely a Phase IIb double blind placebo controlled efficacy study.
http://www.newswire.ca/en/releases/arch ... c5463.html
On the bright side, I had EPO in the pre-clinical stage, but it looks like EPO has already had some phase II trials and is likely to have a phase IIb trial coming up soon, based on the information below (sorry if somebody already posted this and I missed it):
Stem Cell Therapeutics Corp. (SCT), a Canadian biotechnology company engaged in treating central nervous system (CNS) disorders by stimulating endogenous neural stem cells, is pleased to announce that it has entered into an Option to Acquire agreement for up to two additional clinical stage programs, one in schizophrenia and the other in multiple sclerosis. The agreement between SCT and two researchers from the Max
Planck Institute of Experimental Medicine in Germany provides SCT with the right, but not the obligation, to acquire one or both of the clinical stage
programs under option.
The two programs optioned under the agreement also employ EPO as a therapeutic intervention for severe, poorly treated neurological conditions, in this case schizophrenia and multiple sclerosis. If the Option to Acquire is exercised by SCT, the company will have three Phase II clinical programs in progress that employ EPO alone or in combination with other agents for the treatment of serious CNS diseases.
The multiple sclerosis program captured in the agreement has already completed a 24 week open label Phase IIa clinical study seeking improvement in walking distance and Kurtzke Expanded Disability Status Scale (EDSS) efficacy endpoints in chronic progressive multiple sclerosis patients treated with high vs. low doses of EPO. The next clinical development step for the multiple sclerosis program is likely a Phase IIb double blind placebo controlled efficacy study.
http://www.newswire.ca/en/releases/arch ... c5463.html
Riluzole going from phase I to phase II...
Riluzole for Early MS
Neuroprotection with Riluzole in Patients with Early Multiple Sclerosis. CHR Approval Number H9224-29155-01
Dr. Emmanuelle Waubant of the UCSF Department of Neurology is running a study to see if riluzole is safe and effective in treating patients with early Multiple Sclerosis (MS) and Clinically Isolated Syndrome (CIS). The study will evaluate whether riluzole decreases the chance of progression from CIS to MS. You may participate in this research study if you had CIS no more than twelve months ago and if you are 18 through 55 years old.
The drug that we will be testing in this study is a pill called riluzole (Rilutek®). Riluzole was developed by Sanofi-Aventis for treatment of Amyotrophic Lateral Sclerosis (ALS), also known as Lou Gehrig’s disease, a fatal paralyzing disease with an unknown etiology. Riluzole slows neuronal death and as a result, delays the progression of ALS, which is influenced by the death of muscle-controlling nerve cells. Riluzole has been approved by the FDA for treatment of ALS, but it is currently not approved by the FDA for treating CIS or MS.
Approximately forty patients, which were seen at the UCSF MS Center within twelve months of CIS onset, will be enrolled in the study. Patients will be evaluated every month for the first 12 months and every three months thereafter for the total study duration of 24 months. Fifty percent of the patients will receive riluzole, and 50 percent of the patients will receive a placebo (an inactive sugar pill). All patients will start Avonex therapy at month three of the study. The study will be blinded, which means that neither you nor your doctor will know whether you are taking riluzole or a placebo.
http://mscenter.ucsf.edu/research.htm
Riluzole for Early MS
Neuroprotection with Riluzole in Patients with Early Multiple Sclerosis. CHR Approval Number H9224-29155-01
Dr. Emmanuelle Waubant of the UCSF Department of Neurology is running a study to see if riluzole is safe and effective in treating patients with early Multiple Sclerosis (MS) and Clinically Isolated Syndrome (CIS). The study will evaluate whether riluzole decreases the chance of progression from CIS to MS. You may participate in this research study if you had CIS no more than twelve months ago and if you are 18 through 55 years old.
The drug that we will be testing in this study is a pill called riluzole (Rilutek®). Riluzole was developed by Sanofi-Aventis for treatment of Amyotrophic Lateral Sclerosis (ALS), also known as Lou Gehrig’s disease, a fatal paralyzing disease with an unknown etiology. Riluzole slows neuronal death and as a result, delays the progression of ALS, which is influenced by the death of muscle-controlling nerve cells. Riluzole has been approved by the FDA for treatment of ALS, but it is currently not approved by the FDA for treating CIS or MS.
Approximately forty patients, which were seen at the UCSF MS Center within twelve months of CIS onset, will be enrolled in the study. Patients will be evaluated every month for the first 12 months and every three months thereafter for the total study duration of 24 months. Fifty percent of the patients will receive riluzole, and 50 percent of the patients will receive a placebo (an inactive sugar pill). All patients will start Avonex therapy at month three of the study. The study will be blinded, which means that neither you nor your doctor will know whether you are taking riluzole or a placebo.
http://mscenter.ucsf.edu/research.htm
jim4030,
I pasted a story below that appeared on the front page of ThisIsMS earlier this year about Zenapax. It is still going through the clinical trial process for MS, so technically it couldn't be prescribed for MS yet and is probably 5 years away from being approved if it makes it through the clinical trials successfully. On the other hand, it is already an approved drug, so a doctor could prescribe it "off-label", although I doubt that would happen for MS today because of the lack of data. I hope this helps.
Daclizumab Method of Action Surprises Researchers
This story reveals a very important research development that could shed light on the critical question of how and why multiple sclerosis develops (or at least one version of it), and more importantly, how to effectively treat it.
Biogen's Daclizumab has recently surprised researchers with its method of action. Daclizumab, known in the market as Zenapax, is a drug currently used to prevent the rejection of organ transplants, particularly the kidney. It is now being put through Phase II (dosing) trials for multiple sclerosis. When they started the trials, researchers proposed the following hypothesis as to why it might be effective as an MS therapy:
"Interleukin-2 is a natural substance in the body that is necessary for the growth of T-lymphocytes. Zenapax is a genetically engineered antibody that blocks the activity of interleukin-2 and thus interferes with the growth of lymphocytes. Therefore, Zenapax may prevent some of the damage to myelin that occurs in multiple sclerosis."
Remember, in the auto-immune theory of multiple sclerosis, T-lymphocytes are the class of cells often supposed to be the immune system component that has "gone awry" to inadvertently attack myelin.
However, preliminary results in MS patients showed that the drug did not suppress T-cell activity as expected.
"We monitored T-cell function in patients who were injected with the drug, expecting to see that the drug inhibited T-cell function," says Dr. Bielekova.
"We didn't see that at all. To our surprise the T-cells were functioning normally."
The surprise was the fact that daclizumab therapy actually increased the activity of another component of the immune system's natural "killer" cells that are generally targeted at viruses and cancers, and generally only arise in rare circumstances, such as pregnancy (which is another period of quiescent MS activity...). Additionally, the greater the enhancement to this portion of the immune system, the better outcome the patient experienced!
"Not only did the number of regulatory natural killer cells increase in patients treated with daclizumab," says Dr. Bielekova, "but that expansion correlated with the treatment outcome--the more these cells expanded, the better the MS patients did during the trial. And the longer the patients were on the therapy, the more regulatory natural killer cells they had and the better they responded to treatment."
"The best news is that natural killer cells are actually very efficient immune cells that fight viruses or cancers," says Dr. Bielekova (director of University of Cincinnati's Waddell Center for Multiple Sclerosis), "so it appears that daclizumab doesn't damage the immune system. It only shifts the emphasis of the immune reaction from T-cells to natural killer cells.
For referene, an earlier and very small, (10 person), open-label trial indeed suggested some promise: "Daclizumab was very well tolerated and led to a 78% reduction in new contrast-enhancing lesions and to a significant improvement in several clinical outcome measures."
MS is a mystery, involving a complex interplay of immune factors, and even potentially multiple distinct diseases lumped under one name (as cancer was viewed a decade ago). Different treatment modalities may work for different people-- each one of these trials, confounding as they may be in the short-term, will help unravel the overall tapestry.
I pasted a story below that appeared on the front page of ThisIsMS earlier this year about Zenapax. It is still going through the clinical trial process for MS, so technically it couldn't be prescribed for MS yet and is probably 5 years away from being approved if it makes it through the clinical trials successfully. On the other hand, it is already an approved drug, so a doctor could prescribe it "off-label", although I doubt that would happen for MS today because of the lack of data. I hope this helps.
Daclizumab Method of Action Surprises Researchers
This story reveals a very important research development that could shed light on the critical question of how and why multiple sclerosis develops (or at least one version of it), and more importantly, how to effectively treat it.
Biogen's Daclizumab has recently surprised researchers with its method of action. Daclizumab, known in the market as Zenapax, is a drug currently used to prevent the rejection of organ transplants, particularly the kidney. It is now being put through Phase II (dosing) trials for multiple sclerosis. When they started the trials, researchers proposed the following hypothesis as to why it might be effective as an MS therapy:
"Interleukin-2 is a natural substance in the body that is necessary for the growth of T-lymphocytes. Zenapax is a genetically engineered antibody that blocks the activity of interleukin-2 and thus interferes with the growth of lymphocytes. Therefore, Zenapax may prevent some of the damage to myelin that occurs in multiple sclerosis."
Remember, in the auto-immune theory of multiple sclerosis, T-lymphocytes are the class of cells often supposed to be the immune system component that has "gone awry" to inadvertently attack myelin.
However, preliminary results in MS patients showed that the drug did not suppress T-cell activity as expected.
"We monitored T-cell function in patients who were injected with the drug, expecting to see that the drug inhibited T-cell function," says Dr. Bielekova.
"We didn't see that at all. To our surprise the T-cells were functioning normally."
The surprise was the fact that daclizumab therapy actually increased the activity of another component of the immune system's natural "killer" cells that are generally targeted at viruses and cancers, and generally only arise in rare circumstances, such as pregnancy (which is another period of quiescent MS activity...). Additionally, the greater the enhancement to this portion of the immune system, the better outcome the patient experienced!
"Not only did the number of regulatory natural killer cells increase in patients treated with daclizumab," says Dr. Bielekova, "but that expansion correlated with the treatment outcome--the more these cells expanded, the better the MS patients did during the trial. And the longer the patients were on the therapy, the more regulatory natural killer cells they had and the better they responded to treatment."
"The best news is that natural killer cells are actually very efficient immune cells that fight viruses or cancers," says Dr. Bielekova (director of University of Cincinnati's Waddell Center for Multiple Sclerosis), "so it appears that daclizumab doesn't damage the immune system. It only shifts the emphasis of the immune reaction from T-cells to natural killer cells.
For referene, an earlier and very small, (10 person), open-label trial indeed suggested some promise: "Daclizumab was very well tolerated and led to a 78% reduction in new contrast-enhancing lesions and to a significant improvement in several clinical outcome measures."
MS is a mystery, involving a complex interplay of immune factors, and even potentially multiple distinct diseases lumped under one name (as cancer was viewed a decade ago). Different treatment modalities may work for different people-- each one of these trials, confounding as they may be in the short-term, will help unravel the overall tapestry.
So much activity this last week! So many drug annoucements...
Dignan,
You and Ian have been doing a great job of answering my questions which means I will keep asking them.
My neuro mentioned a test with Rebif and cladribine starting in Q1 2007. Can't find cladribine on your list altho I have seen study called CLARITY...I thought CLARITY had already started w/ FDA quick response promised. Did I mix up something that you know of? Also, it turns out that cladribine is a statin. Should that mean something special to me altho I have never heard of this particular one (Leustatin)?
Any info gladly accepted. No research required...I don't understand the really technical responses anyway.
Lee
Dignan,
You and Ian have been doing a great job of answering my questions which means I will keep asking them.
My neuro mentioned a test with Rebif and cladribine starting in Q1 2007. Can't find cladribine on your list altho I have seen study called CLARITY...I thought CLARITY had already started w/ FDA quick response promised. Did I mix up something that you know of? Also, it turns out that cladribine is a statin. Should that mean something special to me altho I have never heard of this particular one (Leustatin)?
Any info gladly accepted. No research required...I don't understand the really technical responses anyway.
Lee
leeeeeway,
The CLARITY study is a phase III study of an oral cladribine formulation called Mylinax, by Serono (it's on the list under phase III). I haven't heard anything about Mylinax and Rebif being tested together, but since they're both Serono products, it makes sense. Sorry I couldn't be more helpful.
The CLARITY study is a phase III study of an oral cladribine formulation called Mylinax, by Serono (it's on the list under phase III). I haven't heard anything about Mylinax and Rebif being tested together, but since they're both Serono products, it makes sense. Sorry I couldn't be more helpful.
A couple of others to add to the pipeline: R411 from Roche in phase I and R348 from Rigel as pre-clinical.
"One negative came as Roche dropped development of DPP-IV R1438 to treat diabetes after Phase II trials. Another candidate, R411, was dropped in asthma but is being tested in Phase 1 trials for multiple sclerosis."
<shortened url>
R348 also has been shown to be selective over other targets in an array of functional assays. In addition, R348 appears to effectively inhibit JAK3-dependent lymphocyte (white blood cell) proliferation, and has demonstrated a good pharmacokinetic profile and oral bioavailability in preclinical studies.
"JAK3 plays a key role in immune cell function and its selective inhibition could provide a targeted therapy for autoimmune diseases such as transplant rejection, multiple sclerosis, rheumatoid arthritis, graft-versus-host disease, and psoriasis. R348 has shown excellent selectivity and efficacy in animal models of immune-mediated disease, and we believe it may be a punctuational advance in treating these diseases," said Donald G. Payan, M.D., executive vice president and chief scientific officer of Rigel.
http://feed.insnews.org/v-cgi/feeds.cgi ... id=2234206
"One negative came as Roche dropped development of DPP-IV R1438 to treat diabetes after Phase II trials. Another candidate, R411, was dropped in asthma but is being tested in Phase 1 trials for multiple sclerosis."
<shortened url>
R348 also has been shown to be selective over other targets in an array of functional assays. In addition, R348 appears to effectively inhibit JAK3-dependent lymphocyte (white blood cell) proliferation, and has demonstrated a good pharmacokinetic profile and oral bioavailability in preclinical studies.
"JAK3 plays a key role in immune cell function and its selective inhibition could provide a targeted therapy for autoimmune diseases such as transplant rejection, multiple sclerosis, rheumatoid arthritis, graft-versus-host disease, and psoriasis. R348 has shown excellent selectivity and efficacy in animal models of immune-mediated disease, and we believe it may be a punctuational advance in treating these diseases," said Donald G. Payan, M.D., executive vice president and chief scientific officer of Rigel.
http://feed.insnews.org/v-cgi/feeds.cgi ... id=2234206
Another one for pre-clinical...
CGEN-54: An antagonistic variant of MCP1 (Monocyte Chemoattractant Protein 1)
MCP1 - also named CCL2 - belongs to the CC protein family and is induced in response to various inflammatory stimuli. Binding of this protein to its cognate receptor, CCR2, leads to the recruitment of specialized immune cells into the site of inflammation, unfortunately often leading to tissue destruction in chronic inflammatory diseases. The Compugen discovered molecule is a novel splice variant of MCP1 which has now been shown to inhibit MCP1 related activity.
The inhibition of the MCP1-CCR2 pathway represents a promising target to effectively modulate disease progression in chronic inflammatory diseases, such as multiple sclerosis. CGEN-54 is a truncated form of MCP1 that was found to antagonize the MCP1-CCR2 pathway both in vitro and in vivo. In cell culture assays, CGEN-54 was shown to inhibit MCP1-induced cell migration, whereas in vivo, CGEN-54 was shown to be effective in reducing experimentally induced peritonitis in mice.
<shortened url>
CGEN-54: An antagonistic variant of MCP1 (Monocyte Chemoattractant Protein 1)
MCP1 - also named CCL2 - belongs to the CC protein family and is induced in response to various inflammatory stimuli. Binding of this protein to its cognate receptor, CCR2, leads to the recruitment of specialized immune cells into the site of inflammation, unfortunately often leading to tissue destruction in chronic inflammatory diseases. The Compugen discovered molecule is a novel splice variant of MCP1 which has now been shown to inhibit MCP1 related activity.
The inhibition of the MCP1-CCR2 pathway represents a promising target to effectively modulate disease progression in chronic inflammatory diseases, such as multiple sclerosis. CGEN-54 is a truncated form of MCP1 that was found to antagonize the MCP1-CCR2 pathway both in vitro and in vivo. In cell culture assays, CGEN-54 was shown to inhibit MCP1-induced cell migration, whereas in vivo, CGEN-54 was shown to be effective in reducing experimentally induced peritonitis in mice.
<shortened url>
Another one I'll add to pre-clinical...
Recovexx: Building on technology developed in the neurology laboratory of Bruce Gold, Ph.D., at OHSU's Center for Research on Occupational and Environmental Toxicology as well as at Vertex Pharmaceuticals Inc., Recovexx is engaged in the development of neurological therapeutics affecting recovery and protection of nerve function. Its key product is Timcodar, a compound with neuroregenerative and neuroprotective biological properties, giving it potential therapeutic value for many neuropathies, including diabetic neuropathy and multiple sclerosis.
http://www.medfordnews.com/articles/ind ... 8&cp=10996
Recovexx: Building on technology developed in the neurology laboratory of Bruce Gold, Ph.D., at OHSU's Center for Research on Occupational and Environmental Toxicology as well as at Vertex Pharmaceuticals Inc., Recovexx is engaged in the development of neurological therapeutics affecting recovery and protection of nerve function. Its key product is Timcodar, a compound with neuroregenerative and neuroprotective biological properties, giving it potential therapeutic value for many neuropathies, including diabetic neuropathy and multiple sclerosis.
http://www.medfordnews.com/articles/ind ... 8&cp=10996
Here's some interesting stuff about a company, Pipex, that is doing estriol trials for MS.
Pipex Completes Reverse Merger, Reports Positive Coprexa Data
Pipex is developing oral Trimesta (estriol) for the treatment of relapsed/remitting multiple sclerosis. The drug, which has completed a Phase II study in that indication, is an estrogenic molecule, approved and marketed in Europe and Asia for the treatment of postmenopausal hot flashes for more than 40 years.
"MS patients who become pregnant have high rates of remission in the third trimester," Kanzer said. "Unfortunately, four to six weeks after delivering, they also have very high rates of relapse of their disease." Estriol - produced only during pregnancy - apparently confers immune benefits on the mother as well as the fetus.
Other investigators completed a 22-month Phase IIa trial that showed "very significant" reductions in the number and size of MS lesions, Kanzer said, and a trial by Pipex will start soon.
<shortened url>
Pipex Completes Reverse Merger, Reports Positive Coprexa Data
Pipex is developing oral Trimesta (estriol) for the treatment of relapsed/remitting multiple sclerosis. The drug, which has completed a Phase II study in that indication, is an estrogenic molecule, approved and marketed in Europe and Asia for the treatment of postmenopausal hot flashes for more than 40 years.
"MS patients who become pregnant have high rates of remission in the third trimester," Kanzer said. "Unfortunately, four to six weeks after delivering, they also have very high rates of relapse of their disease." Estriol - produced only during pregnancy - apparently confers immune benefits on the mother as well as the fetus.
Other investigators completed a 22-month Phase IIa trial that showed "very significant" reductions in the number and size of MS lesions, Kanzer said, and a trial by Pipex will start soon.
<shortened url>
-
CureOrBust
- Family Elder
- Posts: 3374
- Joined: Wed Jul 27, 2005 2:00 pm
- Location: Sydney, Australia
I stumbled accross this LIST.
It seemed pretty long, so i quickly browsed up and down and checked back with your list on two items that sounded new to me. They may be on the list under something else?
MK-0812 http://clinicaltrials.gov/ct/show/NCT00239655 Phase II
ABT-874 http://clinicaltrials.gov/ct/show/NCT00086671 Phase II
there could be more? and the Phase I RG2007, appears to be really called RG2077
It seemed pretty long, so i quickly browsed up and down and checked back with your list on two items that sounded new to me. They may be on the list under something else?
MK-0812 http://clinicaltrials.gov/ct/show/NCT00239655 Phase II
ABT-874 http://clinicaltrials.gov/ct/show/NCT00086671 Phase II
there could be more? and the Phase I RG2007, appears to be really called RG2077