What is the consensus on ruxolitinib and tofacitinib?

[location1]

http://www.dailymail.co.uk/sciencet...-New-drug-reveals-regrowth-mice-ten-DAYS.html

The drugs work by inhibiting a family of enzymes inside hair follicles that are suspended in a resting state, effectively 'waking' the hair. Within 3 weeks, mice that received topical ruxolitinib or tofacitinib had regrown nearly all their hair (right photo; drug was applied only to the right side of the mouse). Little to no hair growth occurred in control mice during the same timeframe (left photo).

The results look amazing and the drugs are already approved for humans (just not for hairloss).

Is anyone gonna give this a try topically?

 

[dusty]

It's a mouse study...if only everything that has worked on mice actually worked on humans

 

[Captain Hook]

These drugs are all tyrosine kinase inhibitors, have a look at the side effect profile for oral use and you'll be scared off for sure. Topically wouldn't be viable because of a few reasons. First being we have no idea as to what vehicle to use and with that no clue as to how well it absorbs and if it absorbs well, who's to say it doesn't enter systemic circulation and cause similar side effects to oral use?

TKIs are also notoriously expensive, have a flip through the British National Formulary (or Google works too I suppose) and look at the price. Not worth it in my opinion for something experimental with limited evidence as to its efficacy.

 

[location1]

On the other hand though, look at those insane results, plus the fact that the drug already exists on the market...

 

[mpbsux20]

Finasteride is safe as a bank compared to these drugs and this is coming from someone who experienced side effects on Finasteride.

 

[dusty]

Tyrosine Kinase inhibition is not something you want. The phosphorylation of tyrosine is important in many processes in the body including the building of new cells to replace old cells. Insulin also acts on TKs stimulating the storage of glucose as glycogen in muscles for energy. Do not take TKs unless you need to

 

[Sweuser]

Saying ruxolinib and tofacitinib are tyrisine kinase I are not really fair, that's not very specific. They are both JAK I, and I believe the purpose for this thread was due to new papers, also on humans, showing potential cure for AA and MBP.

They are also potentally good topicals beeing less than 100 K-Da.

 

[Captain Hook]

Saying ruxolinib and tofacitinib are tyrisine kinase I are not really fair, that's not very specific. They are both JAK I, and I believe the purpose for this thread was due to new papers, also on humans, showing potential cure for AA and MBP.

They are also potentally good topicals beeing less than 100 K-Da.

Oh hey, I've read Swisstemples' work too!

I'm pretty sure you mean 100 Da. 100 kDa is 100,000 daltons. Not even heparin is that heavy.

The fact that it is less than 500 daltons just means it will be able to penetrate the skin for adequate absorption. At this point in time we only know it works in mice and we have no idea as to the side effects from topical absorption and whether it reaches systemic circulation or not. It's far too early to draw conclusions

(References: http://www.ncbi.nlm.nih.gov/pubmed/10839713)

 

[Sweuser]

Oh hey, I've read Swisstemples' work too!

I'm pretty sure you mean 100 Da. 100 kDa is 100,000 daltons. Not even heparin is that heavy.

The fact that it is less than 500 daltons just means it will be able to penetrate the skin for adequate absorption. At this point in time we only know it works in mice and we have no idea as to the side effects from topical absorption and whether it reaches systemic circulation or not. It's far too early to draw conclusions

(References: http://www.ncbi.nlm.nih.gov/pubmed/10839713)

Ooops, my bad! Guess their not that good topicals

 

[location1]

I still think this is worth testing. Why aren't people testing it? It could be the cure

 

[rogerackroyd]

I still think this is worth testing. Why aren't people testing it? It could be the cure

Maybe because one pill costs over 50 bucks?

 

[location1]

Oh really? Well if cost is the only problem, we can surely drive it down because of the volume of people who'll be taking it. If it WORKS, cost is not going to be a problem. We just need something that WORKS.

 

[Captain Hook]

Oh really? Well if cost is the only problem, we can surely drive it down because of the volume of people who'll be taking it. If it WORKS, cost is not going to be a problem. We just need something that WORKS.

Yes really, I mentioned cost in an earlier post in this thread. Not to mention it won't likely be absorbed as a topical (again, reasoning posted in an earlier post). It may work, but take a look at the side effects when taken orally, it makes finasteride look like bubblegum.

 

[Swoop]

It's on mice. So it means totally nada, zero. I don't think it's going to work either in humans. It's apparently very effective to treat AA. However AA is auto-immune driven Androgenetic Alopecia is not. Besides that several compounds that alter the immune response have shown to be effective for AA. I think we would already see evidence of something happening in vivo for Androgenetic Alopecia because the compounds are taken orally and several other JAK inhibitors are running clinical trials. Androgenetic Alopecia is that prevalent in humans that people are automatically a test subject for it. A.M Christiano seems to reason that a topical might enhance the drug concentration in the hair follicles and therefore have a better or other effect. Maybe it would, but again I think we would already see something when these drugs are taken orally. Better lock yourself up in a sterile environment when you take this stuff lol. It's a nasty potentially very dangerous drug.

Some information about penetration & pharmacokinetics; http://www.ncbi.nlm.nih.gov/pubmed/23387374

Dermal penetration of tofacitinib was demonstrated by measurable, although limited, systemic levels of tofacitinib when applied to a treatment area of approximately 1.5% BSA. Mean systemic exposures from the current study were approximately 40-fold lower than exposures from the lowest dose tested (2 mg twice daily) in a previous study of oral tofacitinib in patients with moderate-to-severe psoriasis. Furthermore, the highest individual AUC for ointment 1 and ointment 2 was more than eightfold lower than the mean systemic exposure from the 2 mg twice daily oral tofacitinib dose