Cancer drug could fight hairloss

[swingline747]

http://www.nbcnews.com/health/health-news/cancer-drug-could-be-baldness-remedy-too-n450256

 

[c_super2]

wow. hellouser was right to test these drugs on male pattern baldness suffers. Anyway anyone can test the topical versions on people? What about the pill version?

 

[g.i joey]

pill version is way too dangerous! theyve known this for a while now that the pill version of this drug could completely cure hairloss, the risks are not worth it. topical version does seem appealing though.

 

[kigoma]

My summary. Dr. Christiano has also started a new company related to this:

http://www.hairlosscure2020.com/hug...ould-also-regrow-hair-in-androgenic-alopecia/

 

[Mach]

I thought Pfizer had this. They have numerous JAK inhibitors in trail. They have a cream in phase 2 called Xeljanz. Nothing for hair loss. This seems to be nasty stuff that makes finasteride look like m&ms.

This could be unrelated to Dr.Christiano. last fall she filed some patents for JAK inhibitors. Find those in the Google patent search feature.

 

[I.D WALKER]

Thanx for link Kigoma
What the nice author says is not exactly original, however the potential for JAK inhibitors remains compelling to say the least.
I had to laugh when the author raised his opinion from 3/10 to 5/10. It's better ha ha, but it's sort of like the worn out (rhetorical) joke , "Fifty percent chance of rain in tomorrow's forecast."
We all can agree that new and better treatment may or may not happen, but will we live long enough to enjoy their advantages in our lifetime?
I appreciate the positive attitude and forward moving trending in this area all the same. I suppose cure/better therapy prospects could be worse. (-:

My summary. Dr. Christiano has also started a new company related to this:

http://www.hairlosscure2020.com/hug...ould-also-regrow-hair-in-androgenic-alopecia/

 

[Mr White]

Thanx for link Kigoma
What the nice author says is not exactly original, however the potential for JAK inhibitors remains compelling to say the least.
[...]

I know Dr Christiano's work and I trust her.

Any JAK inhibitor already on the market that we can try?

 

[benjt]

Angela Christiano and colleagues at Columbia University have been testing them as treatments for a rare form of hair loss called alopecia areata.

We were discussing JAK inhibitors already one year ago. As of now, there is no indication that they will work for androgenetic alopecia/male pattern baldness at all.

 

[I.D WALKER]

It might be that I'm a little soft towards buxom, foxy looking academic women, lol but I truly believe Dr. Christiano's professional ethics and abilities are inscrutable.
Nothing commercially available relating to Janus Kinase Inhibitors that I could/would recommend.
My background is not Pharmacology and my opinion is just that.

I know Dr Christiano's work and I trust her.

Any JAK inhibitor already on the market that we can try?

- - - Updated - - -

Bigger hair and exuding much confidence! The happiest beginning and end of our story haha.

 

[Swoop]

We were discussing JAK inhibitors already one year ago. As of now, there is no indication that they will work for androgenetic alopecia/male pattern baldness at all.

Agree. Mice again...

 

[Ventures]

Do you agree that low Vitamin D level and Androgenetic Alopecia are correlated in a certain way. That would explain high prevalence of male pattern baldness among northern European populations. If you look at Arabic population, middle east, emigrants, they all tend to have thick healthy hair http://s1.ibtimes.com/sites/www.ibt...le_large/public/2015/07/20/syria-refugees.jpg

Of course that might just have with their genes meaning they have DHT resistant scalp hair as every bald man has mostly DHT resistant occipital hair, but I think, who knows, maybe sun exposure is correlated to growth inhibitors/prohibitors in male pattern baldness cycles.

 

[whatwhat]

Do you agree that low Vitamin D level and Androgenetic Alopecia are correlated in a certain way. That would explain high prevalence of male pattern baldness among northern European populations. If you look at Arabic population, middle east, emigrants, they all tend to have thick healthy hair http://s1.ibtimes.com/sites/www.ibt...le_large/public/2015/07/20/syria-refugees.jpg

Of course that might just have with their genes meaning they have DHT resistant scalp hair as every bald man has mostly DHT resistant occipital hair, but I think, who knows, maybe sun exposure is correlated to growth inhibitors/prohibitors in male pattern baldness cycles.

The third guy has visible male pattern baldness and his temples have fully receded

 

[ryan82]

Also, there isn't a good rat or mouse model of male pattern baldness." Drugs on the market to grow hair were all discovered by accident — Propecia was found to grow hair as a side-effect of treating enlarged prostates, and Latisse, sold to grow eyelashes, was discovered as a side-effect of a glaucoma treatment

FINALLY THEY UNDERSTAND!! There isn't a rat model fit for human hairloss!

 

[Swoop]

Also, there isn't a good rat or mouse model of male pattern baldness." Drugs on the market to grow hair were all discovered by accident — Propecia was found to grow hair as a side-effect of treating enlarged prostates, and Latisse, sold to grow eyelashes, was discovered as a side-effect of a glaucoma treatment

FINALLY THEY UNDERSTAND!! There isn't a rat model fit for human hairloss!

Oh trust me they already know this for ages lol.

 

[ryan82]

Oh trust me they already know this for ages lol.

:jump:

 

[Dench57]

People tried Tofacitinib a year ago with little success. Considering it has half life of 3 hours...would this not mean it would need to be applied repeatedly throughout the day?

 

[Swoop]

People tried Tofacitinib a year ago with little success. Considering it has half life of 3 hours...would this not mean it would need to be applied repeatedly throughout the day?

http://www.pharmaceutical-journal.c...ign-and-development-of-drugs/20065576.article

 

[Dench57]

http://www.pharmaceutical-journal.c...ign-and-development-of-drugs/20065576.article

Can't see the full article. Whats the gist of it?

 

[Swoop]

Can't see the full article. Whats the gist of it?

http://webcache.googleusercontent.c...5576.article+&cd=1&hair loss=nl&ct=clnk&gl=nl try this.

The take of it is that a drug can have a low half life but stay bound to it's target for longer. RU58841 has only a half life of 1 hour, yet seems to work by 1x daily application. If we look at finasteride;

Finasteride undergoes extensive hepatic metabolism to essentially inactive metabolites, which are eliminated through the bile and urine. The terminal elimination half-life (t1/2z) is 4.7 to 7.1 hours; but despite this, slow accumulation occurs with multiple doses. Values of t1/2z are higher in elderly men, but no dosage adjustments are necessary. Likewise, no dosage adjustments are necessary for patients with renal dysfunction, since the metabolites which accumulate are relatively inactive and well tolerated, and because greater faecal excretion of the metabolites occurs in these patients. The effect of hepatic dysfunction on the metabolism of finasteride is unknown. Therapeutic doses of finasteride produce a rapid and pronounced effect in reducing both plasma and prostate tissue levels of DHT. Doses below 0.5 mg/day do not produce much suppression of DHT levels, and doses above 5 mg/day have little additional benefit. A single dose of finasteride suppresses serum DHT levels for up to 4 days, longer than would be expected from the serum terminal elimination half-life (t1/2z) of the drug: this is probably due to the high affinity that finasteride has for the 5 alpha-reductase enzyme.

The low half life doesn't make sense with the long suppression of DHT that finasteride can induce with a single dose. Now the above study mentions that it is probably due to "high affinity". But that's wrong. It's not affinity that makes this happen the article explains that;

However, researchers have tended to focus on the strength of the binding between a drug candidate and its target (the affinity), rather than on how long the drug remains bound to the target (the residence time). The affinity of a drug is the concentration at which 50% of the target receptors are occupied. This is the ratio of K [SUB]off[/SUB] to K [SUB]on[/SUB] but says nothing about the binding kinetics. “Initially, researchers believed that if a drug has good affinity, it would have a good effect. But this is not the case,” says IJzerman. “You can have a good website, but if you don’t stick to its pages long enough, you probably won’t have learnt that much.”

In short half life, affinity and binding kinetics (residence time) are not the same.