follicept - what's this?

[MoolahLea]

I particularly believe this could be a game changer too. But, I am being careful with getting my expectations high. And this is only cause I lack the technical knowledge that goes into all this science, meaning I am not an expert in this domain. Monday is fast approaching! Can't wait! Devon, I am praying that it does work... Just went for a trip with a bunch of friends, and trust me.. the balding jokes were just off the charts. hahaha... Gets to me sometimes, despite telling myself not to worry about it.

[serenemoon]

LOL. Boldy, by far the most knowledable member this forum has, just KILLED Follicept in his post. Not with some broscience a la 'think of a big pizza', but with REAL science. He explained you guys why the hairless mouse grew hair (these mice were modified to miss mitogen and then they gave back that mitogen and of course then the telogen phase kicks in). And he showed you guys scientific proof that IGF-1 is actually the growthfactor the LEAST associated with hair growth, in *VIVO* proofed in *human clinical trials*. And all you can come up with is a dumb remark like you just posted ... What a joke.

I won't lie, Boldy's argument is powerful. Now, I don't know if there is an argument against this or not, and maybe we will only get a real answer to this after the Follicept trial results, but his argument definitely made me think and was really well put together. Really eager to hear what Follicept has to say about what he said, from a scientific point of view.

[serenemoon]

@boldy,

You are talking about fully senescent cells which is complete norwood 7 stuff. For somebody with some miniaturisation or norwood 3, the product could prove to be superior to anything available at the moment.

If that is the case, then Follicept should work well. I was not sure of the "definition" of senescnent..but if it only applies to severe baldness, then that is great.

[Sogeking]

If that is the case, then Follicept should work well. I was not sure of the "definition" of senescnent..but if it only applies to severe baldness, then that is great.

I would have to agree with Boldy though. And basically the only problem I have with all of this is:

2. That the trial is run in-house privately, there can be some conflict of interest if the results are not as expected, and the product still need to be released.

.

As for the senescent cells in our scalp, no one can tell with certainty that NW3 doesn't have senescent cells. Basically all of the areas on the scalp that are completely bald could have senescent cells.

However if follicept is completely transparent about the results or lack thereof it is still nice someone is actually trying.

I guess this could be closed in a matter of month or two unlike waiting for something for a year to see if it actually does something as it is the case with Bimatoprost.

[sdsurfin]

Hey guys,

This post will contain facts mainly for informational purpose for the readers of this site, not to discourage the owners of this product or what so ever. I think that it is important to stay with both feet on the ground, and stay realistic. I respect the effort put into this project, and am not sure where it went wrong. Weather it was just an over enthusiastic entrepreneur who had some connections to a professor who didn't gasp the difference between mice and human, or lack of research, but it does not matter, still respect for the try.

Follicept Quote 1:

1). No reason to find the results on a CD Hairless mice compelling. It is just confirmation of this initial study: http://www.nature.com/jid/journal/v1.../5603603a.html

Let’s be clear about some facts here.
- IGF1 is a mitogen, it is pro proliferation.
- CD hairless mice is mutated, which prevent the cells, from among others to proliferate, see below

http://www.criver.com/products-servi...d-hairless-rat
Therefore, the mutation in the CR rat abrogates cell proliferation in the hair matrix and affects keratinocyte differentiation in the HF and interfollicular epidermis, a phenotype that is completely distinct from hr/hr. To test whether the CR rat harbored a mutation in the hr gene, we analyzed the coding region of this gene and consensus intron splice site sequences in mutant rats and found no mutation, further supporting phenotypic evidence that the hairless phenotype in CR rats is not allelic with hairless. Finally, using intragenic polymorphisms, we were able to exclude homozygosity at the hairless locus by use of genotypic analysis. Thus, morphologic analysis of successive stages of phenotype development in the CR hairless rat, together with definitive molecular studies, indicate that this mutation may be unique among the other hypotrichotic rat mutations.

- So you take a fresh mice, with fresh cells (not affected telomerase in contrast to AGA Calls) mice that lacks among others a strong mito genic, and feed it with a mitgogen, as results the fresh cells proliferate, and kick start the telogen phase/ matrix proliferation.

2 problems with that approach.
1. You take a mice with fresh cells, fresh telomere, which is mutated, and misses a mitogen, you give it a mitogen, and telogen phase kicks in, very logical.
2. This does not translate to human AGA cells, I will show you why.
http://www.nature.com/jid/journal/v1...id201528a.html
a. In short, without running into details, aga is the result of senescenced cells. Yes it starts with excess AR in the DP in the affected area, however ROS and lack / up regulation of factors, cause senescenced (aged) cells. These cells lack the ability to proliferate, or do anything, and have basically 2 choices.
i. They destroy themselves (apoptosis)
ii. They just sit there without any faction in growth arrest. And start to affect nearby cells with negative signals.
You can’t just add igf1 to aga aged cells. IGF1 is a recognized factor in aging, refer to this study for example: http://www.ncbi.nlm.nih.gov/pubmed/22877754




With other words, you can’t just ad IGF1 only, if you want to protect your cells. Instead you start with express damaging of what is left of the DNA. Result of physically destroyed mitochondria(which is responsible for the energy metabolism within the cell.


Let’s say or assume your “special” vehicle is as good as injection or proved nano liposomal delivery, which proved to deliver molecules/compounds bigger than 7 kda into the dermal layer, then we still have to cope with some failed human trials with IGF1, or stronger, more preferable mitogenics. See table below:




You might want to adjust your formula now and make follicept V2 with FGF2, however that is tried too, at low and high doses.
On the other forum we tried IGF1, FGF2 ,fgf7 ,fgf10 in Nano solution at 2- 25 ppm, 2 people injected IGF / FGF2 without result unfortunately about 2-3 years ago, As noobs we didn't know why back then, but now we understand why.

Some notes from my side:
Without running in to conclusion, 1. I find it worrying that some new posters pop up and start defending this hype like their life depend on it. 2. That the trial is run in-house privately, there can be some conflict of interest if the results are not as expected, and the product still need to be released.
Outsourcing the trial and preferably letting some trusted members participate is more of a hassle, but the only way to gain trust in my opinion. Perhaps this issue can be addressed by follicept.

Good luck all!

Although some of this might make sense, lot of this is also pretty off base or very loosely tied together. don't have time right now to explain all of it, but ill address more later. I have read some of Boldy's posts in the past, and although like swooping you have some understanding of AGA and are good at linking lots of articles and information, I don't find your ability to make sense of it all to be all that insightful. Most of the stuff on cell senescence makes no sense as a counter argument to why this might work. Cells go senescent (die) because of a lack of the proper proteins and growth factors. IGF-1 is unlikely to completely revive dead hair cells, as there is scarring involved and many channels have been broken, but delivering the proper factor at the proper intervals for people with thinning hair can probably prevent cells from senescing or turn around cells that are halfway there. rogaine is used on cells that are dying as well, and the ways it releases certain chemicals turns this process around. same with fin, some regrowth happens because cutting off the negative chemicals lets the cells be nourished and stop dying. In this sense Im not sure what boldy's argument is.

True, the IGF-1 could be a less potent on human follicles than on mice, but that has not been proven yet. you say that hairless mice are missing a mitogenic factor, and that human cells are not. this is exactly what follicept is addressing. androgens are setting off a chain of reactions in people that cuts off the mitogenic factors in the follicle. it's the same problem, except the mice are genetically programmed NOT to ever grow hair, while balding humans can sort of grow hair but some of the mitogenic factors are being hampered. Cell senescence is the end product of all aging and diseases really, but it is not "the cause" of AGA. AGA is caused by genetic constructs that lead the androgen receptor to set off a chain of chemicals that in turn cause cells to die. The point of follicept and other treatments is to halt this dying.

b) As far as injections are concerned I'm really not sure that injecting growth factors into the scalp is the same as using follicept's vehicle. I pretty sure Dr. Hsu has addressed this in the past. While I definitely harbor some skepticism about just how important IGF-1 is to balding until it is used in humans, I'm not sure that even an injected study has ever been carried out for balding. The fact that there are anecdotes of forum people indiscriminately injecting this stuff into the bloodstream and were unsuccessful,does not guarantee that follicept won't work. If anything the graph you posted shows that all these growth factors did indeed have an effect on hair growth. I myself have a hunch that there might be better factors to use than IGF-1, or maybe a mix would be best, but this is definitely a good start, especially as related to inducing anagen (something that has been shown very clearly as something that IGF-1 does). Dr. Hsu wants to start simple and see what happens. He understands the science of this much better than I do and certainly much better than anyone else on here, and if he thinks its worth a shot then Im very interested.

c) as far as the in house trials, this is all nonsense. what company do you really expect to outsource their trials? They can trial this effectively and as simply/cheaply as possible, and involving a mass of crazy forum users is of no value in the initial stages. No one owes you guys anything, and demanding follicept to do this or do that is not only unrealistic, but also indicative of an entitled attitude that belies the young age or psychological malfunction of a lot of forum users. If their trials were to be botched it would not be hard to tell, and there has been no indication that these guys are anything but an upstanding crew. And even if these guys were scammers,which they aren't, you can always NOT BUY. If you know so much about hair loss or are so skeptical, you still have control of your own mind/pocketbook. all follicept is on here to do is get some useful feedback and hopefully start building a customer base should their product work. If they are a scam then so is every other company that sells anything to anyone. everyone wants to build a good product and market it effectively. but not all are as open and generous with their info as follicept has been, which is why its cool that there is a hair loss startup. if you'd rather have only huge universities and big pharmas working on this, with all the interests that they have to represent, all the hurdles they have to jump through, etc, then you are all pretty dumb. this grassroots action is good whether it works or not.

[NeedHairASAP]

Hey guys,

This post will contain facts mainly for informational purpose for the readers of this site, not to discourage the owners of this product or what so ever. I think that it is important to stay with both feet on the ground, and stay realistic. I respect the effort put into this project, and am not sure where it went wrong. Weather it was just an over enthusiastic entrepreneur who had some connections to a professor who didn't gasp the difference between mice and human, or lack of research, but it does not matter, still respect for the try.

Exhibit 1:


ATM regulates insulin-like growth factor 1-secretory clusterin (IGF-1-sCLU) expression that protects cells against senescence.

Abstract
Downstream factors that regulate the decision between senescence and cell death have not been elucidated. Cells undergo senescence through three pathways, replicative senescence (RS), stress-induced premature senescence (SIPS) and oncogene-induced senescence. Recent studies suggest that the ataxia telangiectasia mutant (ATM) kinase is not only a key protein mediating cellular responses to DNA damage, but also regulates cellular senescence induced by telomere end exposure (in RS) or persistent DNA damage (in SIPS). Here, we show that expression of secretory clusterin (sCLU), a known pro-survival extracellular chaperone, is transcriptionally up-regulated during both RS and SIPS, but not in oncogene-induced senescence, consistent with a DNA damage-inducible mechanism. We demonstrate that ATM plays an important role in insulin-like growth factor 1 (IGF-1) expression, that in turn, regulates downstream sCLU induction during senescence. Loss of ATM activity, either by genomic mutation (ATM-deficient fibroblasts from an ataxia telangiectasia patient) or by administration of a chemical inhibitor (AAI, an inhibitor of ATM and ATR), blocks IGF-1-sCLU expression in senescent cells. Downstream, sCLU induction during senescence is mediated by IGF-1R/MAPK/Egr-1 signaling, identical to its induction after DNA damage. In contrast, administration of an IGF-1 inhibitor caused apoptosis of senescent cells. Thus, IGF-1 signaling is required for survival, whereas sCLU appears to protect cells from premature senescence, as IMR-90 cells with sCLU knockdown undergo senescence faster than control cells. Thus, the ATM-IGF-1-sCLU pathway protects cells from lethality and suspends senescence.



Exhibit 2:

Insulin-like growth factor-1 regulates the SIRT1-p53 pathway in cellular senescence

Summary
Cellular senescence, which is known to halt proliferation of aged and stressed cells, plays a key role against cancer development and is also closely associated with organismal aging. While increased insulin-like growth factor (IGF) signaling induces cell proliferation, survival and cancer progression, disrupted IGF signaling is known to enhance longevity concomitantly with delay in aging processes. The molecular mechanisms involved in the regulation of aging by IGF signaling and whether IGF regulates cellular senescence are still poorly understood. In this study, we demonstrate that IGF-1 exerts a dual function in promoting cell proliferation as well as cellular senescence. While acute IGF-1 exposure promotes cell proliferation and is opposed by p53, prolonged IGF-1 treatment induces premature cellular senescence in a p53-dependent manner. We show that prolonged IGF-1 treatment inhibits SIRT1 deacetylase activity, resulting in increased p53 acetylation as well as p53 stabilization and activation, thus leading to premature cellular senescence. In addition, either expression of SIRT1 or inhibition of p53 prevented IGF-1-induced premature cellular senescence. Together, these findings suggest that p53 acts as a molecular switch in monitoring IGF-1-induced proliferation and premature senescence, and suggest a possible molecular connection involving IGF-1-SIRT1-p53 signaling in cellular senescence and aging.



Exhibit 3:

IGF-1 Enhances Expression of iPS Cell Reprogramming Factors and Telomerase activities in Human Dermal Fibroblasts: A potential Role for IGF-1 in Induction of Pluripotent Stem Cells and Antisenescence

Background: Reprogramming somatic cells into induced pluropotent stem cells (iPS) using transcription factors (Oct4, Sox2, Klf4 and c-myc) offers a novel approach for regenerative medicine. However, the iPS cell generation has several obstacles, including the poor efficiency of iPS reprogramming and frequent re-entry of iPS cells into the stage of senescence during passage. Insulin-like growth factor (IGF-1) and its downstream phosphoinositide 3-kinase (PI3K) signaling pathway may maintain the proliferative potential of stem cells. This study was to test the effects of IGF-1 on iPS cell generation and senescence.

Conclusion: IGF-1 may enhance expression of programming factors and telomerase activities in human dermal fibroblasts transduced into iPS cells, while inhibiting expression of the senescence-inducing protein p53. The effects of IGF-1 may be mediated by the PI3 kinase/Akt pathway. Our data demonstrate that the novel biological effects of IGF-1 on iPS generation, and may allow development of an enhanced therapeutic option by employing iPS for treating cardiovascular diseases.



Exhibit 4:

Abstract
The accumulation of senescent stromal cells in aging tissue changes the local microenvironment from normal to a state similar to chronic inflammation. This inflammatory microenvironment can stimulate the proliferation of epithelial cells containing DNA mutations which can ultimately lead to cancer. Using geriatric skin as a model, we demonstrated that senescent fibroblasts also alter how epithelial keratinocytes respond to genotoxic stress, due to the silencing of IGF-1 expression in geriatric fibroblasts. These data indicate that in addition to promoting epithelial tumor growth, senescent fibroblasts also can promote carcinogenic initiation. We hypothesized that commonly used therapeutic stromal wounding therapies can reduce the percentage of senescent fibroblasts and consequently prevent the formation of keratinocytes proliferating with DNA mutations following acute genotoxic (UVB) stress. Sun-protected skin on the lower back of geriatric human volunteers was wounded by dermabrasion and the skin was allowed to heal for three months. In geriatric skin, we found that dermabrasion wounding decreases the proportion of senescent fibroblasts found in geriatric dermis, increases the expression of IGF-1, and restores the appropriate UVB response to epidermal keratinocytes in geriatric skin. Therefore, dermal rejuvenation therapies may play a significant role in preventing the initiation of skin cancer in geriatric patients.





Exhibit 5:

Bioactive IGF-1 release from collagen–GAG scaffold to enhance cartilage repair in vitro


Abstract
Tissue engineering is a promising technique for cartilage repair. Toward this goal, a porous collagen–glycosaminoglycan (CG) scaffold was loaded with different concentrations of insulin-like growth factor-1 (IGF-1) and evaluated as a growth factor delivery device. The biological response was assessed by monitoring the amount of type II collagen and proteoglycan synthesised by the chondrocytes seeded within the scaffolds. IGF-1 release was dependent on the IGF-1 loading concentration used to adsorb IGF-1 onto the CG scaffolds and the amount of IGF-1 released into the media was highest at day 4. This initial IGF-1 release could be modelled using linear regression analysis. Osteoarthritic (OA) chondrocytes seeded within scaffolds containing adsorbed IGF-1 deposited decorin and type II collagen in a dose dependent manner and the highest type II collagen deposition was achieved via loading the scaffold with 50 μg/ml IGF-1. Cells seeded within the IGF-1 loaded scaffolds also deposited more extracellular matrix than the no growth factor control group thus the IGF-1 released from the scaffold remained bioactive and exerted an anabolic effect on OA chondrocytes. The effectiveness of adsorbing IGF-1 onto the scaffold may be due to protection of the molecule from proteolytic digestion allowing a more sustained release of IGF-1 over time compared to adding multiple doses of exogenous growth factor. Incorporating IGF-1 into the CG scaffold provided an initial therapeutic burst release of IGF-1 which is beneficial in initiating ECM deposition and repair in this in vitro model and shows potential for developing this delivery device in vivo.



Exhibit 6:

GW25-e4120 IGF-1 Inhibits Apoptosis of Vascular Smooth Muscle Cells Through PI3/Akt Pathway

In this report, we show that the signaling cascade involved in IGF-1 protectes VSMC against Apop-1-induced apoptosis, while PDGF has no effect. In addition, pretreatment of Apop-1 transfected VSMCs with phosphatidylinositol-3-kinase inhibitor wortmannin, or infection with an adenoviral construct expressing the dominant negative Akt gene (Adeno-dnAkt) blocked the cytoprotective effect of IGF-1, whereas the MEK inhibitor PD98059 had no effect. Conversely, infection with an adenoviral construct expressing the constitutively active Akt (Adeno-MyrAkt) gene, protected VSMC from apoptosis induced by Apop-1 even in the absence of IGF-1, suggesting that IGF-1 prevents VSMC apoptosis induced by Apop-1 through activation of the PI3K/Akt pathway. Furthermore, IGF-1 elevated phospho-Akt expression in Apop-1 transfected VSMCs and Apop-1 decreased phospho-Akt expression. Importantly, IGF-1 inhibited cytochrome c release from mitochondria and blocked activation of intrinsic initiator caspase-9 in Apop-1 transfected VSMCs




Exhibit 7:



Abstract

Apoptosis and cell proliferation are two important cellular processes that determine the accumulation of pulmonary artery smooth muscle cells (PASMC) during pulmonary arterial hypertension (PAH). Insulin-like growth factor 1 (IGF-1) is an endocrine and autocrine/paracrine growth factor that circulates at high levels in the plasma and is expressed in most cell types. IGF-1 has major effects on development, cell growth and differentiation, also tissue repair. Inducible nitric oxide synthase (iNOS) has been shown to serve many vasoprotective roles in vascular smooth muscle cells (VSMCs) including inhibition of VSMC proliferation and migration and stimulation of endothelial cell growth. In this study, we investigated the involvement of iNOS in the process of IGF-1-induced inhibition of PASMC apoptosis. We also examined the role of p38 mitogen-activated protein kinase (MAPK) in the IGF-1-induced iNOS activation. Our results show that exogenous IGF-1 induced the up-regulation of iNOS in PASMC. Immunofluorescence of IGF-1 and iNOS showed a decreased immunostaining of both IGF-1 and iNOS in the cytoplasm and the perinucleus under serum deprivation condition. iNOS inhibition in PASMC in vitro markedly induced IGF-1-mediated anti-apoptosis as assessed by the cell viability measurement, Western blot, mitochondrial potential analysis and nuclear morphology determination. A p38 MAPK inhibitor blocked all the effects of IGF-1 on iNOS. Our findings suggest that IGF-1 inhibits cells apoptosis in PASMC by activating the p38 MAPK–iNOS transduction pathway. This mechanism may contribute to the accumulation of PASMC in early human PAH.




Exhibit 9:



Myostatin, a TGF-β family member, is associated with inhibition of muscle growth and differentiation and might interact with the IGF-1 signaling pathway. Since IGF-1 is secreted at a bioactive level by adipose tissue-derived mesenchymal stem cells (ASCs), these cells (ASCs) provide a therapeutic option for Duchenne Muscular Dystrophy (DMD). But the protective effect of stem cell secreted IGF-1 on myoblast under high level of myostatin remains unclear. In the present study murine myoblasts were exposed to myostatin under presence of ASCs conditioned medium and investigated for proliferation and apoptosis. The protective effect of IGF-1 was further examined by using IGF-1 neutralizing and receptor antibodies as well as gene silencing RNAi technology. MyoD expression was detected to identify impact of IGF-1 on myoblasts differentiation when exposed to myostatin. IGF-1 was accountable for 43.6% of the antiapoptotic impact and 48.8% for the proliferative effect of ASCs conditioned medium. Furthermore, IGF-1 restored mRNA and protein MyoD expression of myoblasts under risk. Beside fusion and transdifferentiation the beneficial effect of ASCs is mediated by paracrine secreted cytokines, particularly IGF-1. The present study underlines the potential of ASCs as a therapeutic option for Duchenne muscular dystrophy and other dystrophic muscle diseases.



Exhibit 10:


Abstract
Objective
Insulin-like growth factor 1 (IGF-1) increases the growth of cultured hair follicles and plays a role in regulating hair migration during the development of hair follicles in transgenic mice. However, the exogenous effect of IGF-1 on hair growth in wild-type mice has not been reported. In the present study, we examined whether IGF-1 was an important regulator of hair follicle growth in wide-type mice in vivo.

Design
C57BL/6 mice were injected with different concentrations of IGF-1 on dorsal skin. The treated tissues were analyzed by immunoassay methods for TGF-β1 and BrdU.

Results
Local injection of IGF-1 increased hair follicle number and prolonged the growing phase during the transition from anagen to telogen. Meanwhile, immunology analyses revealed that IGF-1 also stimulated the proliferation of follicle cells in anagen of the matrix and down regulated TGF-β1 expression in hair follicles.

Conclusions
These observations suggest that IGF-1 is an effective stimulator of hair follicle development in wide-type mice in vivo and may be a promising drug candidate for baldness therapy.


Exhibit 11:


Abstract
Reactive oxygen species (ROS)-induced oxidative stress increases in skeletal muscle with aging and decreases the viability of implanted cells. Type 1 insulin-like growth factor (IGF-1) promotes the survival of skeletal muscle cells under oxidative stress. It is unknown whether IGF-1 protects muscle-derived stem cells (MDSCs) from oxidative stress. In this study, we genetically engineered rat MDSCs to overexpress IGF-1 and determined cell viability, apoptosis, and VEGF secretion under oxidative stress. Overexpression of IGF-1 prevented MDSCs from H2O2-induced caspase-dependent apoptotic cell death by upregulating the PI3K/AKT pathway, accompanied with an increase of NF-κB, p-NF-κB, Bcl-2, and VEGF, as well as a decrease of Bax. In contrast, pre-administration of picropodophyllinb, wortmannin, 1L-6-hydroxymethyl-chiro-inositol-2-((R)-2-O-methyl-3-O-octadecylcarbonate), or pyrrolidine-dithiocarbamate, specific inhibitors of IGF-1R, PI3K, AKT, and NF-κB, respectively, followed by treatment with H2O2, resulted in cell death of MDSCs. Our data indicated that IGF-1 suppresses apoptosis and enhances the paracrine function of MDSCs under oxidative stress via enhancing IGF-1R/PI3K/AKT signaling. Thus, IGF-1 gene-modified MDSCs present a potential application in the treatment of muscle wasting, such as urethra intrinsic sphincter deficiency.

[sdsurfin]

and none of what i said is a claim that follicept will definitely work. Again, I have no idea. But the reasons that have been stated for it NOT to work are all at pretty badly thought out. My biggest concern is that the death of HF cells hinges on several channels, including inflammatory processes, and I'm not sure IGF-1 is enough to offset/fix the other channels. It really all depends on how much influence it has on hair growth in people. Past studies have suggested in plays a large role, but without testing this with follicepts new vehicle, none of us can really say how successful/not it can be. In short, unless you are a pro hair researcher, and as with any medical progress, just hang tight, shut up and wait.

[serenemoon]

Thanks for the explanation sdsurfin!! Makes sense.

[nameless]

@Boldy, The company's reason for not giving experimental samples to the forum members is reasonable and logical. The company's point is that it's risky and irresponsible to send out experimental medicines through the mail to people the company is many many miles away from, that the company has not conducted baseline workups on and have not been medically cleared for taking this experimental medicine. What do you think Merk would have said if you asked Merck to let forum members be in the original propecia studies through the via mail with no medical workups and no baseline established? What would Glaxo have said if you asked them to do the same with dutasteride? What if you had asked the same of Upjohn for the original Rogaine studies? It wouldn't happen Boldy. Responsible professional drug company personnel would reject that proposal. And by the way, the proponent of that idea is Arishi, and yes I mean the same Arishi who bashes Nigam for marketing cell-based experimental treatments to people before all of the kinks are worked out of cell-based hair loss treatments. So Arishi has a long history of bashing Dr. Nigam for doing exactly what Arishi is trying to pressure Follicept into doing here.

Boldy, if I was Devon I would reject the idea too. It's risky and it's unprofessional.

That having been said, I need a chance to read through your scientific points before I can comment on those issues. But just so you know, I am HIGHLY doubtful that Follicept will work. That aside,

1. The arguments that the company has perpetrated a fraud are thus far unfounded.

2. It is totally reasonable for the company to reject the idea of allowing forum members to test their product vial the mail. As a matter of fact, if the company did agree to do that then they would not be following industry protocol and they would be taking needless, irresponsible, and reckless risks.

3. IGF-1 in a topical might get into the follicles better than IGF-1 injected because injected IGF-1 would likely shoot straight in and permeate the follicles directly in the path of injection only whereas topically applied IGF-1 could theoretically get into virtually all the follicles since the topical solution would be spread over the entire scalp.

4. I also think that it's hard to imagine that IGF-1 alone can reverse hair loss as well or better than Rogaine. At minimum I think that they may need to add more growth factors.

5. I also have concerns about whether or not the company is using a potent enough dose of IGF-1. I get the sense that the dose is low.

6. I also have concerns because they are using e.coli IGF-1 rather than human IGF-1.

[Keki]

I wonder where are all those studies of igf-1 injected on human and their results, seems everybody is using increlex from ages but 0 proof, only anedoctal stuff from few user in bodybuilder forums or people who actually injected themself chinese stuff but 0 complete study on this argument, and it's very strange, my idea is people actually injected themself with real crap and actually no one on earth know what's the real effect of igf-1 on human scalp at this point