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What arava does.....pubmed


#1

1: FEBS Lett. 1993 Nov 15;334(2):161-4. Links
Inhibition of the epidermal growth factor receptor tyrosine kinase activity by leflunomide.Mattar T, Kochhar K, Bartlett R, Bremer EG, Finnegan A.
Department of Immunology, Johannes Gutenberg University, Mainz, Germany.

The active metabolite of leflunomide, A77 1726 inhibits the proliferation of a variety of mammalian cell lines in culture. Epidermal growth factor (EGF)-dependent proliferation is inhibited by A77 1726 at an effective dose of 30-40 microM. A77 1726 appears to directly inhibit the EGF receptor tyrosine-specific kinase activity both in intact cells and purified EGF receptors at the same effective dose. These data suggest that leflunomide inhibits cellular proliferation by the inhibition of tyrosine-specific kinase activities.

PMID: 8224241 [PubMed - indexed for MEDLINE]

obviouly it inhibits egf through an indirect route, through inhibition of tyrosine kinease activity…if you look around online, it apparently is pretty good for arthritis, unless much of what Ive read is corporate spam…


#2

Benji you are getting obsessed with EGF …aint you ?


#3

» Benji you are getting obsessed with EGF …aint you ?

Amilcar, by blocking epidermal growth factor during the healing process post abrasion, it would seem that we would be “making” the body make new hair follicles. The hair follicle is the command center for skin renewal. The signals to renew and rejuvinate the skin come from parts of the follicle according to Dr. Loren Pickart. This is probably why a follicle is made in response to a wound in animals, who really do need their coats. We are still mammals, albeit very highly evolved ones.

Inhibiting EGF-and thus not allowing skin to be “regrown” in response to the abrasion, is probably the most important factor in that patent to be honest.

Amilcar, I want this to work. If neither follica or acell (and probably many many of the same pathways are being activated in these approaches) works, it really may be a long long time before any real “new” hair can be grown. We’d be back to manual transplantation to be honest. HM is not a given. Look at it this way…HM has been worked on at ICX and Aderans in earnest since at least 2002. The initial discovery was in 1984 as TAGOHL has pointed out. Growing hair cells outside the body in tissue matrices aside, Im beginning to wonder if cell-inject HM is going to work at all. It really would be nice if follica or acell can turn this trick, because if they cant…it really may be a long while, and I dont want that, do you?


#4

It should be noted that some antiandrogens reduce the concentration of EGF

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=9759701


#5

benji, I understand perfectly your point.

You have already mentioned a point about a further enhancement of this approach if its going to work aka : silencing genes that would make new follicules androgen sensitive thus during the “window of opportunity” (neogenesis) .I wonder if you read that stanford study in which scientists were perfectly capable of silencing any gene they wanted while keeping the others active. My point is that this in conjunction with (Acell/Follica) might be the way to go for creating the REAL FINAL CURE. Of course we need to find in a definite way the genes to blame

PS :
ACELL and FOLLICA both try to TRICK the body and prevent it from healing and thinking its a wound that it just needs to treat it according to the standard procedure


#6

So is (oral) Arava anywhere near as functional at the EGF-R inhibition as doing the job with the real Gentifib?