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Senior Member
Originally Posted by Jens1986
PSK 3841, a nonsteroidal
antiandrogen, has completed phase IIa
trials for the treatment of androgenetic
alopecia and a clinical proof-of-concept
study to reduce sebum flow and
secretion in patients with acne. Six
months of treatment with PSK 3481
demonstrated equivalent or better net
hair growth compared with finasteride.
Source: «Drug News» Vol. 13, No. 13 March 2004
Wow 2004! How depressing :'( All our problems would have been solved if this came out...sigh
Let's just hope we don't add Histogen to this list. They've now been silent for 15 months after completion of Phase 2a
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Interesting, its a shame I'm only a nw 2/3 otherwise I would apply as I am close to the area.
Isn't Desmond from Australia or the oceanic region? Or was another forum regular
Edit: Here's another one...RK-023. There is not much info on it but its currently being trialed on eye lashes with the intended effect to turn velus hairs into something more so it seems.
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Originally Posted by huawei
Interesting, its a shame I'm only a nw 2/3 otherwise I would apply as I am close to the area.
Isn't Desmond from Australia or the oceanic region? Or was another forum regular
Edit: Here's another one...RK-023. There is not much info on it but its currently being trialed on eye lashes with the intended effect to turn velus hairs into something more so it seems.
Seems phase IIa was complete in januari 2011:
The completion of the Phase 2a clinical study of RK-023 for the treatment of androgenetic alopecia has been announced in January 24th, 2011.
http://www.businesswire.com/news/hom...3#.UvuptfldW1s
Although it seems they made a new formula of Rk-023, as they started Phase I in February 2011.
Don't know why, but it's automatically changed to dutch.
http://www.news-medical.net/news/201...096/Dutch.aspx
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Originally Posted by Desmond84
Wow 2004! How depressing :'( All our problems would have been solved if this came out...sigh
Let's just hope we don't add Histogen to this list. They've now been silent for 15 months after completion of Phase 2a
PSK 3841 = RU 58841, got renamed after Roussel Uclaf sold it to ProStrakan.
It was just to show hellouser that RU made it past Phase I
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Originally Posted by Jens1986
PSK 3841 = RU 58841, got renamed after Roussel Uclaf sold it to ProStrakan.
It was just to show hellouser that RU made it past Phase I
It still got shelved in the end. Nothing to be happy about.
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Originally Posted by hellouser
It still got shelved in the end. Nothing to be happy about.
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"
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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/NCT02275351
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Originally Posted by thinning44
I'm very curious. We know the WNT/b-catenin pathway plays a immense role in hairloss. Hopefully this direct agonist of the WNT pathway will do a better job than minox for example as a growth agent.
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Originally Posted by Swooping
I'm very curious. We know the WNT/b-catenin pathway plays a immense role in hairloss. Hopefully this direct agonist of the WNT pathway will do a better job than minox for example as a growth agent.
it also play a role in the adipose cells differentiation: http://www.pnas.org/content/111/15/E1501.abstract
and we know that the fatty tissue ;required also for hair growth; on our scalps is thinning as we lose our hair.
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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.
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