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Some news


#1


http://www.iguanabio.com/hey-daphne-zohars-follica-on-foxnews/


#2

» http://www.foxnews.com/story/0,2933,509799,00.html

Yes but not particularly encouraging news, read the last paragraph in the article:

"A patent is now out for this process of follicle neogenesis, and a company called Follica Inc., which includes scientists in the original wounding experiment, is heading up the project. While the treatment is still years away, and may cross paths with the idea of hair multiplication, pre-clinical trials are already underway.

Baldness be gone: There is no determinable date as to when this might be available given that trials can last years. As soon as 2015 or 2018 could be a possibility, but that’s being generous."


#3

Wonder what happened to 3 to 4 years if not sooner broadcast? The hair is no doubt a very complex subject.


#4

» Wonder what happened to 3 to 4 years if not sooner broadcast? The hair is
» no doubt a very complex subject.

Can someone tell me what is low-dose topical EGFR inhibitors


#5

FDA trials generally take a decade to bring most anything to market.

You can listen to all kinds of other predictions if you want. But they don’t mean jack sh*t, not even coming from the people involved in the project itself.


#6

only one or two years ago, we all thought HM is just 3 years or something away. now its 10 years. wow, damn…


#7

» only one or two years ago, we all thought HM is just 3 years or something
» away. now its 10 years. wow, damn…

After reading “Baldness be gone: Intercytex predicts treatment to be available within five years (before 2013).” in that article I don’t care what it says about anything else, it has to be made up lol.


#8

» » only one or two years ago, we all thought HM is just 3 years or
» something
» » away. now its 10 years. wow, damn…
»
» After reading “Baldness be gone: Intercytex predicts treatment to be
» available within five years (before 2013).” in that article I don’t care
» what it says about anything else, it has to be made up lol.

Exactly. The company is on the verge of bankruptcy. The author of that article did 15 minutes of on-line research and then wrote the article. Totally uninformed. It does show that ICX was really good at doing one thing: press releases. Whoever their PR person was, they earned their money (the only one on the whole staff to do so).


#9

» Can someone tell me what is low-dose topical EGFR inhibitors

Here you go, great reading material if you can’t sleep at night :slight_smile:

the whole patent for EGFR inhibitors

http://www.wipo.int/pctdb/en/wo.jsp?WO=2008042216&IA=US2007020842&DISPLAY=DESC

In one aspect, the invention features a composition including from 0.001% to 0.1% (w/v) of a small molecule EGFR inhibitor formulated for topical administration, wherein the EGFR inhibitor is a non-naturally occurring nitrogen-including heterocycle of less than about 2,000 daltons, or a metabolite thereof. hi another aspect, the invention features a kit including (i) a composition including from 0.000001% to 10% (w/v) of a small molecule EGFR inhibitor formulated for topical administration, wherein the EGFR inhibitor is a non- naturally occurring nitrogen-including heterocycle of less than about 2,000 daltons, or a metabolite thereof, and (ii) instructions for applying this

composition to the skin of a subject in need of generating a hair follicle or stimulating a hair growth.

The invention further features a kit including (i) a composition of the invention and (ii) instructions for applying the composition to the skin of a subject.

The invention also features a kit including (i) a composition of the invention; and (ii) instructions for applying the composition to the skin of a subject in need of generating a hair follicle or stimulating a hair growth.

The invention features a kit including (i) a composition of the invention; and (ii) instructions for administration of the composition to the skin of a subject, wherein the skin has undergone reepithelialization less than two weeks prior to the first administration of the composition.

The invention features a kit including (i) a composition comprising an EGFR antibody; and (ii) instructions for administering the antibody to a subject in need of generating a hair follicle or stimulating a hair growth. In one embodiment, the antibody is selected from zalutumumab, cetuximab, IMC 11F8, matuzumab, SC 100, ALT 110, PX 1032, BMS599626, MDX 214, and PX 1041.

The invention further features a kit including a composition formulated for topical administration including (i) a small molecule EGFR inhibitor selected from leflunomide, gefitinib, erlotinib, lapatinib, canertinib, vandetanib, CL-387785, PKI166, pelitinib, HKI-272, and HKI-357; and (ii) an additional biologically active agent selected from an antihistamine, an anti-inflammatory, a retinoid, an anti-androgen, an immunosuppressant, a channel opener, an antibiotic, and an antimicrobial. In one embodiment, the small molecule EGFR inhibitor is gefitinib or erlotinib and the additional biologically active agent is a channel opener selected from minoxidil, diazoxide, and phenytoin.

Any of the above kits can optionally include instructions for applying the composition to the head of a subject (e.g., to the scalp, cheek, chin, lower

face, or eyebrow), for applying the composition to the skin of a subject once or twice daily, for applying the composition to the skin of a subject for at least 2, 3, 4, 5, 6, 7, 8, 9, or even 10 consecutive days, for administering the composition during the night, or administering the composition during the day. The invention features a method for generating a hair follicle or stimulating a hair growth on the skin of a subject by (i) disrupting the skin of the subject (for example, resulting in the induction of reepithelialization of the skin of the subject) and (ii) contacting the cells of the skin with a small molecule EGFR inhibitor, or a metabolite thereof, in an amount sufficient to generate hair follicles or stimulate hair growth on the skin. In certain embodiments, step (a) is performed less than two weeks, 10 days, 8 days, 5 days, or even 3 days prior to step (b). In other embodiments, step (a) is performed simultaneous with, or more than one day, two days, 3 days or one week after step (b). The invention further features a method for generating a hair follicle or stimulating a hair growth on the skin of the head of a subject by (i) contacting the cells of the skin with a small molecule EGFR inhibitor, or a metabolite thereof, in an amount sufficient to generate hair follicles or stimulate hair growth on the skin, wherein the EGFR inhibitor is a non-naturally occurring nitrogen-including heterocycle of less than about 2,000 daltons or a metabolite thereof and with the proviso that the skin is not an eyelid.

The invention also features a method for generating a hair follicle or stimulating a hair growth on the skin of a subject by (i) inducing reepithelialization of the skin of the subject; and (ii) contacting the cells of the skin with an EGFR antibody in an amount sufficient to generate hair follicles or stimulate hair growth on the skin.

The invention features a method for generating a hair follicle or stimulating a hair growth on the skin of a subject by (i) inducing reepithelialization of the skin of the subject; and (ii) administering to the

subject an EGFR inhibitor selected from a small molecule EGFR inhibitor, or a metabolite thereof, and an EGFR antibody, wherein the EGFR inhibitor is formulated for sustained release and administered in an amount sufficient to generate hair follicles or stimulate hair growth on the skin. In one embodiment, steps (i) and (ii) are performed concurrently.

The invention further features a method for producing pigmented hair on a subject by (i) generating a hair follicle on the subject according to the method of the invention; and (ii) suppressing an expression of a Wnt protein in the hair follicle. In certain embodiments the step of suppressing an expression of a Wnt protein includes inducing an expression of a Dkkl protein.

Any of the above methods optionally include the step of contacting the skin of the subject with a composition of the invention. -

In one particular embodiment, the methods of the invention include performing the contacting step during the day or performing the contacting step during the night.

In any of the forgoing methods the EGFR inhibitor can be administered systemically or topically.

In any of the forgoing methods the reepithelialized skin lacks a stratum corneum, includes newly formed keratinocytes, or includes embryonic hair follicles exhibiting one or more characteristic markers selected from BerEP4, cytokeratin 15, cytokeratin 17, β-catenin, sonic hedgehog, and alkaline phosphatase.

In an embodiment of the above methods, the method includes generating a hair follicle or stimulating a hair growth on the head, scalp, cheek, chin, or eyebrow of a subject.

For any of the above methods, the subjects can from balding of the scalp, face, or eyebrow. The subject may suffer from a disease associated with balding, such as androgenetic alopecia, discoid lupus erythematosis, congenital hypotrichosis, lichen planopilaris, or scarring alopecia. The methods of the

invention can also produce faster hair growth and thicker hair (in comparison to a subject not undergoing treatment). In another aspect, the composition of any of the forgoing methods of the invention can be administered to the subject once or twice daily (e.g., for at least 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, or more consecutive days).

In a particular embodiment of the methods, kits, and compositions of the invention, the small molecule EGFR inhibitor formulated for topical administration includes 0.000001% to 10%, 0.00001% to 10%, 0.00001% to 1%, 0.0001% to 1%, 0.0001% to 0.5%, 0.001% to 0.5%, 0.01% to 0.5%, 0.1% to 0.5%, or even 0.001% to 0.1% (w/v) of a small molecule EGFR inhibitor.

In another particular embodiment of the methods, kits, and compositions of the invention, the topical formulations include a pharmaceutically acceptable excipient selected from an antioxidant (e.g., thiols, sulphoximines, metal chelators, fatty acids, vitamins (including vitamin E), phenols, stilbenes, uric acid, mannose, selenium, and propyl gallate), an emulsifying excipient (e.g., polyethoxylated fatty acids, PEG-fatty acid diesters, PEG-fatty acid mono-ester and di-ester mixtures, polyethylene glycol glycerol fatty acid esters, alcohol-oil transesterifϊcation products, polyglycerized fatty acids, propylene glycol fatty acid esters, mixtures of propylene glycol esters-glycerol esters, mono- and diglycerides, sterol and sterol derivatives, polyethylene glycol sorbitan fatty acid esters, polyethylene glycol alkyl ethers, sugar esters, polyethylene glycol alkyl phenols, polyoxyethylene-polyoxypropylene block copolymers, sorbitan fatty acid esters, lower alcohol fatty acid esters, ionic surfactants, tocopherol esters, and sterol esters), a gelling agent, a hydrocolloid, a cross-linking agent, and a plasticizer. In one embodiment, the topical formulation can include from 0.5 to 50%, 0.5 to 25%, 0.5 to 15%, 0.5 to 10%, 0.5 to 5%, or 0.5 to 3% (w/w) one or more emulsifying excipients, from 0.5 to 50%, 0.5 to 25%, 0.5 to 15%, 0.5 to 10%, 0.5 to 5%, or 0.5 to 3% (w/w) one or more gelling agents, from

0.001% to 3%, 0.01% to 1%, 0.05% to 0.5% (w/w) one or more antioxidants,

from 0.001% to 3%, 0.01% to 1%, 0.05% to 0.5% (w/w) one or more cross- linking agents, from 0.001% to 3%, 0.01% to 1%, 0.05% to 0.5% (w/w) one or more plasticizers, and from 0.5 to 50%, 0.5 to 25%, 0.5 to 15%, 0.5 to 10%, 0.5 to 5%, or 0.5 to 3% (w/w) one or more hydrocolloids. In yet another particular embodiment of the methods, kits, and compositions of the invention, the EGFR inhibitor (e.g., a small molecule EGFR inhibitor or EGFR antibody) is combined (e.g., administered, formulated, or contained in a kit) with an additional biologically active agent selected from an antihistamine (e.g., mepyramine, diphenhydramine, and antazoline), an anti-inflammatory (e.g., corticosteroids, NTHEs, and COX-2 inhibitors), a retinoid (e.g., 13-cis-retinoic acid, adapalene, all-trans-retinoic acid, and etretinate), an anti-androgen (e.g., finasteride, flutamide, diazoxide, l lalpha-hydroxyprogesterone, ketoconazole, RU58841, dutasteride, fluridil, and QLT-7704), an immunosuppressant (e.g., cyclosporine, tacrolimus, rapamycin, everolimus, and pimecrolimus), a channel opener (e.g., minoxidil, diazoxide, and phenytoin), an antibiotic, and an antimicrobial (e.g., benzyl benzoate, benzalkonium chloride, benzoic acid, benzyl alcohol, butylparaben, ethylparaben, methylparaben, propylparaben, camphorated metacresol, camphorated phenol, hexylresorcinol, methylbenzethonium chloride, cetrimide, chlorhexidine, chlorobutanol, chlorocresol, cresol, glycerin, imidurea, phenol, phenoxyethanol, phenylethylalcohol, phenylmercuric acetate, phenylmercuric borate, phenylmercuric nitrate, potassium sorbate, sodium benzoate, sodium proprionate, sorbic acid, and thiomersal).

In a particular embodiment of the methods, kits, and compositions of the invention, the EGFR inhibitor is administered, formulated, or is part of a kit with an anti-androgen (e.g., finasteride ) and a channel opener (e.g., minoxidil).

In still another embodiment of the methods, kits, and compositions of the invention, the topical formulation is a cream, lotion, stick, ointment, gel, spray, foam, patch, aerosol, wound dressing, or drop.

In an embodiment of any of the forgoing methods, kits, and compositions, the small molecule EGFR inhibitor is selected from leflunomide, the leflunomide metabolite A771726, gefitinib, erlotinib, lapatinib, canertinib, vandetanib, CL-387785, PKI166, pelitinib, HKI-272, and HKI-357. In another embodiment of any of the forgoing methods, kits, and compositions, the EGFR antibody is selected from zalutumumab, cetuximab, IMC 11F8, matuzumab, SC 100, ALT 110, PX 1032, BMS599626, MDX 214, and PX 1041.

The terms “administration” and “administering” refer to a method of giving a dosage of a pharmaceutical composition to a patient, where the method is, e.g., topical, oral, intravenous, transdermal, subcutaneous, intraperitoneal, or intramuscular. The preferred method of administration can - vary depending on various factors, e.g., the components of the pharmaceutical composition, site at which hair growth and hair follicle generation is desired. In the methods, kits, and compositions of the invention, the administration is, desirably, topical.

By “an amount sufficient” is meant the amount of an EGFR inhibitor (e.g., a small molecule EGFR inhibitor or an EGFR antibody) required to increase the rate of new hair follicle generation and/or new hair growth on the scalp or eyebrow of a subject in comparison to the rate of new hair follicle generation or hair growth observed in the absence of treatment. The effective amount of EGFR inhibitor used to practice the present invention varies depending upon the inhibitor being used, the manner of administration, the age, body weight, and general health of the subject. Ultimately, the attending physician, will decide the appropriate amount and dosage regimen. Such amount is referred to as “an amount sufficient.”

As used herein, “reepithelization” refers to the process that occurs during formation of a new epidermis. Tissue undergoing this process can be characterized by the lack of hair follicle morphogenesis, cells in an embryonic-

like state, or by lack of a stratum corneum.

By “disruption” is meant a sufficient amount of disturbance to existing hair follicles and the surrounding epidermis and/or dermis to induce an “embryonic-like” state. This embryonic-like state includes the activation, migration, and differentiation of epithelial stem cells from the bulge region of the hair follicle or the interfollicular epidermis. The depth of skin disruption can include in increasing amounts: partial removal of the stratum corneum, complete removal of the stratum corneum, partial removal of the epidermis, complete removal of the epidermis, partial disruption of the dermis and complete removal of the dermis. Skin disruption can also include disruption of the mid to lower epidermis and/or dermis without any disturbance to the stratum- corneum and/or outer epidermis. Different levels of skin disruption • can be accomplished by chemical, energetic, mechanical, sound, ultrasound, and/or electromagnetic based methods. By “controlled release” is meant the regulated spatial and temporal release of a therapeutic compound from a formulation. The term "controlled release"is meant to include delayed release, sustained release, and release from the formulation in pulses or sinusoidal patterns. In controlled release formulations the V3x may or may not change. The controlled release of the compound may be activated by an exogenous or endogenous stimulus.

By “delayed release” is meant that the therapeutically active component is not immediately released from the formulation (e.g., a carrier particle).

By “sustained release” is meant a form of controlled release whereby the therapeutically active compound is released over an extended period of time. As used herein, “formulated for topical administration” refers to a composition of the invention containing a therapeutic compound and formulated with a pharmaceutically acceptable excipient to form a dispersible composition. Compositions formulated for topical administration (e.g., as a cream, gel, lotion, ointment, microdermabrasion particle, and any other topical

formulation described herein) are those manufactured or sold in accordance with governmental regulations regarding a therapeutic regimen that includes instructions for the topical administration of the composition.

By “small molecule EGFR inhibitor” is meant a molecule that inhibits the function of one or more EGFR family tyrosine kinases. Tyrosine kinases of the EGFR family include EGFR, HER-2, and HER-4 (see Raymond et al., Drugs 60(Suppl.l):15 (2000); and Harari et al., Oncogene 19:6102 (2000)). Small molecule EGFR inhibitors include, for example, gefitinib (Baselga et al., Drugs 60(Suppl. 1):33 (2000)), erlotinib (Pollack et al., J. Pharm. Exp. Ther. 291 :739 (1999)), lapatinib (Lackey et al., 92nd AACR Meeting, New Orleans, abstract 4582 (2001)), canertinib (Bridges et al., Curr. Med. Chem. 6:825 (1999)), vandetanib (Wedge et al., Cancer Res. 62:4645 (2002)), CL-387785 (Discafani et al., Biochem. Pharmacol. 57:917 (1999)), PKI166 (Takada et al., DrugMetab. Dispos. 32: 1272 (2004)), pelitinib (Torrance et al., Nature Medicine 6: 1024 (2000)), HKI-272, HKI-357 (for HKI-272 and HKI-357 see, for example, Greenberger et al., 11th NCI-EORTC-AACR Symposium on New Drugs in Cancer Therapy, Amsterdam, abstract 388 (2000); Rabindran et al., Cancer Res. 64:3958 (2004); Holbro et al., Ann. Rev. Pharm. Tox. 44:195 (2004); Tsou et al., J. Med. Chem. 48:1107 (2005); and Tejpar et al., J. Clin. Oncol. ASCO Annual Meeting Proc. 22:3579 (2004)), and leflunomide


#10

» Wonder what happened to 3 to 4 years if not sooner broadcast? The hair is
» no doubt a very complex subject.

There is no new info in these articles. No new statements from Follica. Nothing.
Its just a journalist picking up the story again and stating whats already been said for the past year!

This future balding treatment is still in the development stages and that’s why you haven’t seen any products on the shelf just yet. However, companies like the Britain-based Intercytex are developing a cell therapy process for male-pattern baldness, and in June 2008, the company announced a successful phase II trial of its hair implantation tests.

Baldness be gone: Intercytex predicts treatment to be available within five years (before 2013).

Anyone who knows anything knows that ICX is dying on its arse and this article is quoting them from a year ago!

Until something new is actually released from a company then its not worth listening to!


#11

only one or two years ago, we all thought HM is just 3 years or something away. now its 10 years. wow, damn…

That belief only worked if the 3-stage clinical trials process would not happen.

That bullsh*t gets predictably sold to people again & again with every new product timeline we hear. Just assume 3 stages = 10 years and you’ll stop being disappointed. Really.

Has ICX really been “stringing everybody along” with delayed timelines?

Study the actual progress on ICX-TRC, and you begin to notice a pattern: They got 2/3rds of the way through the FDA trials, and it took them about 2/3rds of a decade to do it. Start ignoring the total-bullsh*t predictions and suddenly the entire program looks like it’s maintained a predictable schedule for years now.

It’s too bad TRC seems essentially dead now, because they had actually gone pretty far.