You are always so negative. It got shelved cus its not stable enough and/or they didnt think it was good enough for production, fin was allready on the marked and its easier to just take a pill. Its easy to get RU, and if it wasnt for Roussel Uclaf/ProStrakan we would not have RU as an option. Researhers/scientists are helping a lot of us, stop complaining about everything pls it just makes u look like a whiner. "omgomgomg if we were women this would have been fixed a long time ago, the world dont give a shit about men"
Sm04554
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Phase 2 for Samumed SM04554 now posted on clinicaltrials.gov. Multiple US sites listed, not yet recruiting, androgenetic alopecia.
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Phase 2 for Samumed SM04554 now posted on clinicaltrials.gov. Multiple US sites listed, not yet recruiting, androgenetic alopecia.
http://www.clinicaltrials.gov/ct2/show/NCT02275351Comment
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and we know that the fatty tissue ;required also for hair growth; on our scalps is thinning as we lose our hair.Comment
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If i'm correct : wnt agonist works the same way as wnt's, they need the LRP5/6 + frizzled receptor to phosphorylze GSK3b, so that B-cetanin can be trans located to the nuclies, and genes such as tcf(important for hair growth), can be activated.
Now in aga we many inhibitors one of the is DKK1 which block the above mentioned receptor where wnt does its work. GSk3b inhibitors like vpa or more selective 6BIO , don't need the frizzeled + lrp5-6 receptors, it enters the cell, and immediately starts gsk3b phosphorylation of GSK3 that leads to b-cetanin accumulation and translocation to the nuclies(what we need). so it is a shortcut and it overrules the inhibitory effect of dkk1. it is why i believe that gsk3b inhibitors have more potential in vivo.Comment
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If i stand correct: wnt agonist works the same way as wnt's, they need the LRP5/6 + frizzled receptor to phosphorylze GSK3b, so that B-cetanin can be trans located to the nuclies, and genes such as tcf(important for hair growth), can be activated.
now in aga we many inhibitors one of the is DKK1 which block the above mentioned receptor where wnt does its work. GSk3b inhibitors like vpa or more selective 6BIO , don't need the frizzeled + lrp5-6 receptors, it enters the cell, and immediately starts gsk3b phosphorylation of GSK3 that leads to b-cetanin accumulation and translocation to the nuclies(what we need). so it is a shortcut and it overrules the inhibitory effect of dkk1. it is why i believe that gsk3b inhibitors have more potential in vivo.Comment
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Guys they will start having Phase 2 clinical trials. Let's get the word out so members of the community can participate. Maybe Spencer Kobren can look into giving this publicity.
Remember, you cannot be on any HL meds if you want to be part of the trial.Comment
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Also the Phase II trial is recruiting 300 participants, which shows how well funded they are.
I recall reading somewhere they had some sort of agreement with Pfizer.Comment
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