Getfitinib hair growth on nose......probably sunburn also

» Another possibility I have thought of is maybe it was from simply rubbing
» the nose? I know I sometimes give it a good rub if I can feel some dead
» skin or whatever, or maybe she had a cold? Constant blowing into tissues
» can certainly cause a raw nose after awhile… would explain all those
» hairs underneath as well.
» Anyway, just throwing that out there for people trying this when in the
» EGFR inhibitor period to lay off vigorous rubbing of the nose or any other
» body part for unwanted hair…

interesting, the rubbing caused by a cold could explain the bottom of the tip of the nose very well

» » Thank you very much TAGOHL, I just ordered. Am looking forward to trying
» » it for real. Im in this to grow hair…hopefully big-time.
»
» wouldn’t it be better to get a prescription for gefitinib and then get it
» from a reliable source?

Sure, but this option is not practical at all. Unless you have cancer, is there a doctor who is going to do this? Not to mention the cost is prohibitive in the US, where no generic version is available.

You have to do the best you can. It’s pretty much overseas generic, or nothing at all.

BTW, I am nervous about taking gefitinib. While most of the side-effects are simply annoying (acne, rash, diarrhea, etc.), there’s one side-effect associated with its use called interstitial lung disease. It’s a scarring lung disease. Particularly if you are Asian…about 3 Asians in 100 get this side-effect (3%), and it’s fatal about a 1/3 of the time, which means for every 100 people who take gefitinib, one of them dies of this side-effect. The incidence is about 1% for other populations. Perhaps even more concerning is the speed at which this side-effect happens – your lungs can start to scar within hours of the first dose, and within 48 hours the scarring can show up on CT scans. Within a week, you could be dead from it. Granted, this is a rare side-effect, but I always felt that 10 days use would avoid serious side-effects, but this is not true in the case of gefitinib.

» » » Thank you very much TAGOHL, I just ordered. Am looking forward to
» trying
» » » it for real. Im in this to grow hair…hopefully big-time.
» »
» » wouldn’t it be better to get a prescription for gefitinib and then get
» it
» » from a reliable source?
»
» Sure, but this option is not practical at all. Unless you have cancer,
» is there a doctor who is going to do this? Not to mention the cost is
» prohibitive in the US, where no generic version is available.
»
» You have to do the best you can. It’s pretty much overseas generic, or
» nothing at all.
»
» BTW, I am nervous about taking gefitinib. While most of the side-effects
» are simply annoying (acne, rash, diarrhea, etc.), there’s one side-effect
» associated with its use called interstitial lung disease. It’s a scarring
» lung disease. Particularly if you are Asian…about 3 Asians in 100 get
» this side-effect (3%), and it’s fatal about a 1/3 of the time, which means
» for every 100 people who take gefitinib, one of them dies of this
» side-effect. The incidence is about 1% for other populations. Perhaps even
» more concerning is the speed at which this side-effect happens – your
» lungs can start to scar within hours of the first dose, and within 48 hours
» the scarring can show up on CT scans. Within a week, you could be dead from
» it. Granted, this is a rare side-effect, but I always felt that 10 days use
» would avoid serious side-effects, but this is not true in the case of
» gefitinib.

dead but with your hair growing, what’s the problem ?

» Sure, but this option is not practical at all. Unless you have cancer,
» is there a doctor who is going to do this? Not to mention the cost is
» prohibitive in the US, where no generic version is available.

I would add that, personally, I would take this route (i.e., a US doc writing me a prescription, and having it filled at a local pharmacy) if I could find a doc willing to do this, and if I could afford it. But I can’t afford it, and I think I would be hard-pressed to convince a doctor why a healthy man needs to take a lung cancer drug.

» »»
» BTW, I am nervous about taking gefitinib. While most of the side-effects
» are simply annoying (acne, rash, diarrhea, etc.), there’s one side-effect
» associated with its use called interstitial lung disease. It’s a scarring
» lung disease. Particularly if you are Asian…about 3 Asians in 100 get
» this side-effect (3%), and it’s fatal about a 1/3 of the time, which means
» for every 100 people who take gefitinib, one of them dies of this
» side-effect. The incidence is about 1% for other populations. Perhaps even
» more concerning is the speed at which this side-effect happens – your
» lungs can start to scar within hours of the first dose, and within 48 hours
» the scarring can show up on CT scans. Within a week, you could be dead from
» it. Granted, this is a rare side-effect, but I always felt that 10 days use
» would avoid serious side-effects, but this is not true in the case of
» gefitinib.

Yikes, thats pretty heady stuff there. Perhaps I ought to order some Arava and try it first. :expressionless:
One of the reasons I didn’t fear the internal usage of these drugs was the ten day period. Its hard to imagine dying from ten days usage of anything-including chemotherapy.

I wonder if any of the other egf antagonists like erlonitib could be had via the internet?

I have a strong feeling that it will have to be a synthetic indication for this to work. I was reading about milk thistle the other night, and supposedly its metabolized pretty quickly (something like four hours)…The potato protien peptide might be something to look into if all else fails. I can eat a lot of potatoes…:slight_smile:

There are several variables that have run through my mind concerning the getfitinib regrowth photos. I have wondered if it might be alright to take it as soon as wounding is performed. I say this because the two regrowth photos are almost certainly the effect of sunburn. To imagine these folks had too much sun, and then just three or four days later just happened to start taking getfitinib seems statistically unlikely. It would “seem” biologically that if one was burned, and was on a egf-antagonist, that the dermis attempting to “heal” the epidermis would almost be forced to build hair follicles in response. Its something to ponder, but Im probably wrong for whatever esoteric, complicated, biological reason. I sure hope one of us has luck with this. Folks on this forum dont seem to realize (Hangininhthere) that HM has been worked on for many years now and might NEVER be viable enough to put much hair on a human head. I cannot see any other way besides a gene therapy that could put hair on a man’s head. And even gene therapy would have to kick start long-dormat-collagen-encased vellus hairs that have suffered a great deal of immunological damage, etc. as another hurdle. I have an ugly feeling that if Follica or Acell dont work…nothing might.

» » »»
» I have an ugly feeling that if Follica or Acell dont
» work…nothing might.

I agree. Maybe nothing in the next several decades.

As for the Gentifib - They may have regrown hair even without the 3-5 day waiting period after the wound, but that doesn’t mean that keeping the waiting period wouldn’t have improved their results a bunch. (We also don’t know how long it took to grow in those cases, either.)

There’s one other oddball thing that concerns me - and I know this is a remote likelyhood -

But what if the Fin/Dut usage during the forming period somehow HURTS the hairs? Or renders them LESS able to resist androgen exposure than they otherwise would have been?

We know that some people have regrown on Gentifib without androgen suppression. And the hairs seem to live on that way, at least in the short term for sure.

And we know that Folica’s mouse/skin grafts probably didn’t have androgen exposure, but they also weren’t trying to survive in an androgen-rich environment after they were formed, either.

Like I said, not a MAJOR concern, but it’s a little nagging doubt.

» » »»
» » BTW, I am nervous about taking gefitinib. While most of the
» side-effects
» » are simply annoying (acne, rash, diarrhea, etc.), there’s one
» side-effect
» » associated with its use called interstitial lung disease. It’s a
» scarring
» » lung disease. Particularly if you are Asian…about 3 Asians in 100 get
» » this side-effect (3%), and it’s fatal about a 1/3 of the time, which
» means
» » for every 100 people who take gefitinib, one of them dies of this
» » side-effect. The incidence is about 1% for other populations. Perhaps
» even
» » more concerning is the speed at which this side-effect happens – your
» » lungs can start to scar within hours of the first dose, and within 48
» hours
» » the scarring can show up on CT scans. Within a week, you could be dead
» from
» » it. Granted, this is a rare side-effect, but I always felt that 10 days
» use
» » would avoid serious side-effects, but this is not true in the case of
» » gefitinib.
»
»
»
»
»
» Yikes, thats pretty heady stuff there. Perhaps I ought to order some Arava
» and try it first. :expressionless:
» One of the reasons I didn’t fear the internal usage of these drugs was the
» ten day period. Its hard to imagine dying from ten days usage of
» anything-including chemotherapy.
»
» I wonder if any of the other egf antagonists like erlonitib could be had
» via the internet?
»
»
» I have a strong feeling that it will have to be a synthetic indication for
» this to work. I was reading about milk thistle the other night, and
» supposedly its metabolized pretty quickly (something like four
» hours)…The potato protien peptide might be something to look into if
» all else fails. I can eat a lot of potatoes…:slight_smile:
»
»
»
» There are several variables that have run through my mind concerning the
» getfitinib regrowth photos. I have wondered if it might be alright to take
» it as soon as wounding is performed. I say this because the two regrowth
» photos are almost certainly the effect of sunburn. To imagine these folks
» had too much sun, and then just three or four days later just happened to
» start taking getfitinib seems statistically unlikely. It would “seem”
» biologically that if one was burned, and was on a egf-antagonist, that the
» dermis attempting to “heal” the epidermis would almost be forced to build
» hair follicles in response. Its something to ponder, but Im probably wrong
» for whatever esoteric, complicated, biological reason. I sure hope one of
» us has luck with this. Folks on this forum dont seem to realize
» (Hangininhthere) that HM has been worked on for many years now and might
» NEVER be viable enough to put much hair on a human head. I cannot see any
» other way besides a gene therapy that could put hair on a man’s head. And
» even gene therapy would have to kick start long-dormat-collagen-encased
» vellus hairs that have suffered a great deal of immunological damage, etc.
» as another hurdle. I have an ugly feeling that if Follica or Acell dont
» work…nothing might.

Would it be counter-productive to use getfitnib right away instead of waiting 3-4 days post wounding? I mean is there a logical reason why it couldn’t be done other than the patent saying so.?

» » » »»
» » »
»
»
» There’s one other oddball thing that concerns me - and I know this is a
» remote likelyhood -
»
» But what if the Fin/Dut usage during the forming period somehow HURTS the
» hairs? Or renders them LESS able to resist androgen exposure than they
» otherwise would have been?
»
» We know that some people have regrown on Gentifib without androgen
» suppression. And the hairs seem to live on that way, at least in the short
» term for sure.
»
» And we know that Folica’s mouse/skin grafts probably didn’t have androgen
» exposure, but they also weren’t trying to survive in an androgen-rich
» environment after they were formed, either.
»
» Like I said, not a MAJOR concern, but it’s a little nagging doubt.

Ive pondered these things myself, but simply deferred to the patent after I seen anti-androgens included therein. Believe me, I have wondered that if the hair could be “made” with the full compliment of androgens, then perhaps it would be very androgen resistant, etc. I considered also the genetic difference between hirsute men and bald men—the particular variant of the androgen receptor gene. If someone stuck a gun to my head and said “what is baldness and why does it happen and your life is riding on it”, I’d have to reply that bald mens androgen receptors on their hair follicles are genetically different based on them inheriting that gene based on the German study that found that. Whether this makes the receptors work “too well”, or chemically break down slower, or they have more androgen receptors on their hairs (I think that is supposeldy proven in balding scalp now) I cant say for certain, but I think it gets back to that gene. Ive wondered if bald men get androgen receptor genetic expression in their dermal tissue as strong as it is in muscle tissue vs. other men, etc. I thought about all this stuff before, believe me. Since I have no way of testing any of it, I find myself no wiser than before. It would be nice to think that though…we simply have androgen receptors that work too well and not something inherently wrong with our hair. A lot of bald men sure are hairy over the rest of their body. My body hair certainly isn’t deficient in any way. It grows like a motherphucker!!! My muscle tissue certainly isn’t deficient, and even at my age, Im still pretty built up (I was once very “ripped”).

I’d feel alot better if the guy with the getfitinib associated hairgrowth seen his hair grow LONG on his head. It kinda does look like high-quality chest hair in the photo. Bryan Shelton has mentioned a few times that finding the “difference” between why head hair doesn’t like androgens but body hair does might be the key to baldness. I suppose if we could ‘change’ the response of head hair to androgens, all those vellus hairs on our heads would awaken and grow like your body hair begins to post-pubtery. BUT…would it look like head hair and not body hair? Ive thought about all this stuff in my mind in the past…

Another thing about follica that is a mild concern is the fact that you will be making more sebaceous glands up there…and making more oil along with the vellus hair’s sebaceous glands which are just as big as they ever were. If follica really works extremely well, the hair removal method of which they speak might be able to be performed beforehand in bald scalp to get rid of the old vellus hairs first before making new hairs. Will the hairs come in follicular units? Will they all be single hairs? There is so much to think about.

Like you…if Follica and ACELL (to be honest, based on the animal photographs Ive seen, ACELL is probably as promising a method as there is…for the donor area of a man’s head anyway) both fail…we are probably going to be better off forgetting it. I think it will be a long time before HM is good enough to sell myself. I mean hell, Jahoda, as TAGOHL has mentioned, made that discovery back in the damned 80s, and the technology still isn’t good enough to sell yet? Thats very problemmatic to me. Some of these naysaysers had really better hope these last two methodologies can be made to go, because it they cant…they are screwed

I’d feel alot better if the guy with the getfitinib associated hairgrowth seen his hair grow LONG on his head. It kinda does look like high-quality chest hair in the photo. Bryan Shelton has mentioned a few times that finding the “difference” between why head hair doesn’t like androgens but body hair does might be the key to baldness. I suppose if we could ‘change’ the response of head hair to androgens, all those vellus hairs on our heads would awaken and grow like your body hair begins to post-pubtery. BUT…would it look like head hair and not body hair? Ive thought about all this stuff in my mind in the past…

I don’t really worry much about getting body-type hair on the head. If the hairs are genetically programmed, they should come out the same. It’s one thing to stop something from working correctly, but I think a switch like that (for example, the difference in reactions to androgens) would be something different entirely. Same reasoning why I don’t worry about characteristics.

As for the sebacious glands, I don’t know what to think about that.

I guess I just mentally group all that stuff into “the body will follow the right instructions that it was born with” and leave it at that.

Maybe that’s stupid of me, but it seems to be pretty common across the body’s systems. There’s a lot of ways to make something not form and/or function correctly, but it’s hard to make the body do anything DIFFERENTLY.

And the body does have a lot of (correctly formed) regeneration ability built into it in general. The skin more than any other area.

» Would it be counter-productive to use getfitnib right away instead of
» waiting 3-4 days post wounding? I mean is there a logical reason why it
» couldn’t be done other than the patent saying so.?

Well, over-expressing Wnt the whole way doesn’t seem to be an issue. Wound healing doesn’t appear to get compromised, yet more follicles are created post-healing. This is based on the mice experiments in the original Cotsarelis paper.

With EGF, it’s less clear. EGF plays a role in normal wound healing, and if you start suppressing it right way, you may get altered wound healing. Whether this is really something to be concerned about, I don’t know. But in theory, it’s one reason why you would wait.

The literature on this topic is a little contradictory (there is no abstract for the first study):

Wound healing is not impaired by the epidermal growth factor receptor-tyrosine kinase inhibitor gefitinib. Ann Oncol. 2003 Aug;14(8):1330-1.

The epidermal growth factor receptor (EGFR): role in corneal wound healing and homeostasis. Exp Eye Res. 2001 May;72(5):511-7.

To evaluate the role of the epidermal growth factor receptor (EGFR) in corneal epithelial wound healing, the effect of an EGFR inhibitor on epithelial cell proliferation and cell stratification during wound healing was investigated. From 3 days prior to wounding until wound healing was complete, rats were systemically treated with either an EGFR tyrosine kinase inhibitor (ZD1839) at 40 mg kg(-1) day(-1)or 80 mg kg(-1) day(-1), or with vehicle only (control). A single corneal wound was made in the center of 66 rat corneas, using a 6.0 mm glass tube wrapped in tissue paper soaked in n-heptanol. Subsequently, each wound was photographed and measured by a computer-assisted digitizer every 12 hr. To determine the number of cells in S phase, entire corneas were labelled with (3)H-thymidine and subjected to autoradiography at 0, 12, 24 and 48 hr after wounding. Epithelial thickness was also measured at these time points by microscopy. Epithelial wound healing was significantly and dose-dependently delayed following administration of ZD1839. At 24 hr after wounding, the number of S-phase cells in the limbal corneal epithelium was significantly lower in both the treated groups compared with the control group (P < 0.05). In the cornea before wounding (0 hr) and at 48 hr post-wounding, epithelial thickness was also significantly less in treated rats compared with controls (P < 0.05). These results indicate that EGFR inhibition affects epithelial cell proliferation and stratification during corneal epithelial wound healing and may play a role in maintaining normal corneal epithelial thickness. Copyright 2001 Academic Press.

PMID: 11311043 [PubMed - indexed for MEDLINE]

» Yikes, thats pretty heady stuff there. Perhaps I ought to order some Arava
» and try it first. :expressionless:

Erlotinib can cause interstitial lung disease, too. Even Areva can cause it – there are reports in the literature of multiple people who’ve taken leflunomide and subsequently died from this side-effect. The link seems to be the EGF receptor. Inhibiting the EGFR can be dangerous if you have pre-existing lung damage, say from raditation therapy or smoking. If I was an Asian who smoked, I wouldn’t consider taking gentifib, erlotinib, or leflunomide orally for something like hair loss. What makes this even more of a concern is A) lung scarring can happen very rapidly when exposed to these drugs, B) by the time you get the first symptoms, it’s too late, the damage is already done, and C) sometimes the damage is irreversible or fatal, even after stopping the drug.

I realize I’m just being paranoid. After all, the risk is low, and if you have healthy lungs, you are probably fine. But it’s reminder that we’re not playing around with completely benign drugs.

» I have wondered if it might be alright to take
» it as soon as wounding is performed.

Maybe. I just posted a study which, at least from the title, seemed to indicate that gefitinib doesn’t adversely effect wound healing. I don’t know if there would be any subsequent effect on the ‘embryonic window’.

» » Yikes, thats pretty heady stuff there. Perhaps I ought to order some
» Arava
» » and try it first. :expressionless:
»
» Erlotinib can cause interstitial lung disease, too. Even Areva can cause
» it – there are reports in the literature of multiple people who’ve taken
» leflunomide and subsequently died from this side-effect. The link seems to
» be the EGF receptor. Inhibiting the EGFR can be dangerous if you have
» pre-existing lung damage, say from raditation therapy or smoking. If I was
» an Asian who smoked, I wouldn’t consider taking gentifib, erlotinib, or
» leflunomide orally for something like hair loss. What makes this even more
» of a concern is A) lung scarring can happen very rapidly when
» exposed to these drugs, B) by the time you get the first symptoms, it’s too
» late, the damage is already done, and C) sometimes the damage is
» irreversible or fatal, even after stopping the drug.
»
» I realize I’m just being paranoid. After all, the risk is low, and if you
» have healthy lungs, you are probably fine. But it’s reminder that we’re not
» playing around with completely benign drugs.
»
» » I have wondered if it might be alright to take
» » it as soon as wounding is performed.
»
» Maybe. I just posted a study which, at least from the title, seemed to
» indicate that gefitinib doesn’t adversely effect wound healing. I don’t
» know if there would be any subsequent effect on the ‘embryonic window’.

How did you know I was smoking Asian? LOL!

I really would imagine Follica doesn’t want to run the risks associated with internal egf-receptor antagonists legally, so they are probably having to tinker with them to get acceptable topical formulations of them that dont interefere with the healing process. Who knows if all of these drugs can be matched with carriers that will keep them in the correct skin level and not be systemically absorbed, and yet still work.

In other words, Follica is probably having to get involved with pharmacology even though they dont want to in association with getfitinib, erlonitib, etc. Thats going to take time to trial, check for internal side effects, etc. No wonder they seemingly are putting the brakes on it and slowing the projections down.

If one in 100 men had an unacceptable side effect (lung disease), that equates with 10 per 1,000, and 100 per 10,000, and 10,000 per million. I dont think lawsuits from 10,000 men with serious lung disease would be economically feasible. Its likely a good ten million men would get follica if it really worked pretty well, so that would come out to 100,000 guys with lung disease. Nobody could afford legal bills that would ensue from something like that.
Simply put, they are probably working on topical formulations of these EGF-recetor drugs and making sure they can work and not have internal side effects at the moment, hence why they aren’t rushing into trials. Testing the efficacy and safety alone in conjuntion with their procedure would seemingly burn at least several months…

I thought I read a pretty fair amount about Leflunomide, but I hadn’t heard about all that.

I know this lung issue is a rare one, but is it something that’s a total Y/N question? Or could it do lesser degrees of lung damage to a higher percentage of users than just the ones that actually drop dead?

My lungs are fine, and I’d take my chances if it’s all or nothing. But if it’s also 20% likely to do 10% damage to my lungs, etc . . . that’s another story entirely.

» I know this lung issue is a rare one, but is it something that’s a total
» Y/N question? Or could it do lesser degrees of lung damage to a higher
» percentage of users than just the ones that actually drop dead?

Well, here’s a brand new paper on leflunomide and lung injury. It’s worth the read, for sure. About 1 in 82 people who took leflunomide developed lung damage. About 1 in 210 people died from lung damage induced by leflunomide.

What really bugs me about this side-effect is that by the time you realize something is wrong, you’re already screwed. And by screwed, I mean your lungs are scarred.

Mod Rheumatol. 2008 Jun 13. [Epub ahead of print]

Proposals for leflunomide use to avoid lung injury in patients with rheumatoid arthritis.

Among the 5,043 consecutive patients registered in the postmarketing surveillance for leflunomide, 61 were reported to have lung injury and 24 died from it. The adjusted multivariate logistic regression analysis of the risk factors showed that preexisting interstitial lung disease posed the greatest risk, as well as loading dose, smoking history, and low body weight of 40 kg or less with odds ratios of 8.17, 3.97, 3.12, and 2.91, respectively. In 12 patients, lung injury developed even 2 months after leflunomide withdrawal. When patients with (n = 9) and without (n = 13) fatal outcome were compared, eight out of the former, and six out of the latter had preexisting interstitial lung disease; the former showed severe hypoxemia, high serum C-reactive protein level, hypoalbuminemia, and continuous lymphocytopenia, and required mechanical ventilation. On the basis of these results and literature review, the committee proposes that leflunomide should only be recommended as a second-line drug, should not be administered to patients with preexisting interstitial lung disease, should also not be administered to patients with smoking history or those with low body weight, and should be administered without loading dose. Careful monitoring is necessary, and when lung injury develops, leflunomide elimination using colestyramine is mandatory.

PMID: 18551351 [PubMed - as supplied by publisher]

» » I know this lung issue is a rare one, but is it something that’s a total
» » Y/N question? Or could it do lesser degrees of lung damage to a higher
» » percentage of users than just the ones that actually drop dead?
»
» Well, here’s a brand new paper on leflunomide and lung injury. It’s worth
» the read, for sure. About 1 in 82 people who took leflunomide developed
» lung damage. About 1 in 210 people died from lung damage induced by
» leflunomide.
»
» What really bugs me about this side-effect is that by the time you realize
» something is wrong, you’re already screwed. And by screwed, I mean your
» lungs are scarred.
»
» Mod Rheumatol. 2008 Jun 13. [Epub ahead of print]
»
» Proposals for leflunomide use to avoid lung injury in patients with
» rheumatoid arthritis.
»
» Among the 5,043 consecutive patients registered in the postmarketing
» surveillance for leflunomide, 61 were reported to have lung injury and 24
» died from it. The adjusted multivariate logistic regression analysis of the
» risk factors showed that preexisting interstitial lung disease posed the
» greatest risk, as well as loading dose, smoking history, and low body
» weight of 40 kg or less with odds ratios of 8.17, 3.97, 3.12, and 2.91,
» respectively. In 12 patients, lung injury developed even 2 months after
» leflunomide withdrawal. When patients with (n = 9) and without (n = 13)
» fatal outcome were compared, eight out of the former, and six out of the
» latter had preexisting interstitial lung disease; the former showed severe
» hypoxemia, high serum C-reactive protein level, hypoalbuminemia, and
» continuous lymphocytopenia, and required mechanical ventilation. On the
» basis of these results and literature review, the committee proposes that
» leflunomide should only be recommended as a second-line drug, should not be
» administered to patients with preexisting interstitial lung disease, should
» also not be administered to patients with smoking history or those with low
» body weight, and should be administered without loading dose. Careful
» monitoring is necessary, and when lung injury develops, leflunomide
» elimination using colestyramine is mandatory.
»
» PMID: 18551351 [PubMed - as supplied by publisher]

I have a 25% TCA peel (which will not feel nice) and Topicaine (Lidocaine gel, 4%) that eases pain. Would it not just be friggin’ sweet if those two would do the trick?

Note on the topicaine however, the instructs say no hair removal is to have taken place for three weeks leading up to its usage for whatever reason.

I feel pretty certain that given the side effects, gel or foam formulations of egf-inhibitors that are still prescript only are being worked on by Follica as we speak. This is probably why they aren’t flying into trials right now. I re-looked at experiment 7 in the patent and noted that they did subsequent experiments with human skin, finding they could replicate the result over and over. They know it works outside of the human immune system doing “something” to nullify it in donor-area scalp skin. They’d already be testing this with cyclosporin if the immune system was their only concern. I think the lung side effect is the “something else” that is holding it up…just my two cents.

Good post, benji.

With the number of people who will ultimately be treated with this procedure (assuming it works, of course), they will want a topical that doesn’t leak systemically, yet can still reach therapeutic concentrations in the skin. I’ll have to look at the range they gave in the patent for the topical dose of EGFR inhibitors.

So it sounds like Leflunomide’s damage was raised when the dose was prpoprtionally higher (like in same dose but smaller body weight), but I don’t see any other real controllable factor to assume it’s not gonna happen to me if I try this stuff orally.

Man, 1 in 82 is a hell of a high incidence to assume it’s safe. The way that paper shakes out, I’m not convinced it’s not just damaging EVERY users’ lungs. But maybe the damage is only showing up in clearly testable amounts in 1/82nd of the users, especially those with bad lungs or small bodies to feel it more.

This makes me wanna forget a Leflunomide try, and go straight to trying to make a topical out of something. It may ruin my chances of putting the questions to rest about Folica working, but it’s better than lung damage or death.

How hard can it be to do that, anyway?

Either the stuff absorbs throught the skin with relatively normal carriers or it doesn’t, right? Isn’t the question of absorbtion mostly just about the drug itself?

And also, either topically-applied amounts of Gentifib or Leflunomide are a systemic risk or they’re not, right? Assuming the same amount is absorbed and working topically, then I don’t think a topical’s formulation has much shot at changing the systemic characteristic one way or the other, right?

I would expect Gentifib to be a better try than Leflunomide just because of previous info about the drugs and Folica’s actions.

Anybody have thoughts about all this stuff?

» »
» »
»
»
»
»
»
»
» Either the stuff absorbs throught the skin with relatively normal carriers
» or it doesn’t, right? Isn’t the question of absorbtion mostly just about
» the drug itself?
»
» And also, either topically-applied amounts of Gentifib or Leflunomide are
» a systemic risk or they’re not, right? Assuming the same amount is
» absorbed and working topically, then I don’t think a topical’s formulation
» has much shot at changing the systemic characteristic one way or the
» other, right?
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You bring up the same concerns I have…This is almost assuredly what Follica is working on right now…a topical formulation that isn’t systemically absorbed in some human skin model that still works in the dermis…that must be the reason they haven’t raced to a trial yet.

Ive posted a patent concerning “natural” EGF-antagonists. Soy isoflavones apparently inhibit egf…soy isoflavone gel caps can be obtained and could perhaps be used topically. Lidocaine gels exist (I have a bottle) that could be obtained topically. I dont smoke and have (to my knowledge) healthy lungs. I ordered getfitinib two days ago. If it gets here…I’ll probably still give it a shot. Perhaps I ought try the lidocaine and soy isoflavones first (behind the other ear).

I wish ACELL would hurry up and test their thing…:slight_smile:

We will either roll snake eyes with this stuff or get nada for the next decade in my opinion. Thats why Im excited about it. I just dont see anything else working in anywhere near the near term.
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you really still wanna try the stuff orally now? Is Gentifib less of a risk then Leflunomide for the lung issue or something?

I dunno.

I agree that a 85-out-of-5043 risk doesn’t really seem that high. But I’d feel a hell of a lot more ballsy about trying this stuff if I knew the rest of the 4958 patients didn’t get ANY lung damage for sure. It just sounds like this could be a shades-of-gray problem with any usage, like I suspect is the deal with Finasteride and sexual side effects.

And the study also really shoots down the loading-dose standard procedure for Leflunomide. For all I know it might take weeks to get the effect functionally up to our needed levels without that. If the EGF-R inhibition has to be started by a few days after the wound, you’d need to have started that way ahead of time just to make it work at all. Either that or you at least compromise the strength of the loading dose.

How does Gentifib stack up?

Is the lung issue of the same kind of frequency/severity as Leflunomide seems to produce?

Is the loading dose necessary with Gentifib (and if not, maybe it’s just that much more risky when starting it than Leflunomide)?

Honestly I don’t have a lot of faith in the natural EGF-R inihbitors. Folica spelled out that it had to be unnatural in their eyes. And more importantly I just think it’s much more likely to have been stumbled upon by now if there was an effective natural alternative. The “Folica method” might not have been around for centuries, but plenty of people have gotten skin injuries while taking natural substances. I just feel like we should have a little more anecdotal evidence of it if this was possible.