Curis, P&g, And The Lost Baldness Cure

[Photon]

I think that dose is too high. My results slowed down on higher doses too. I'm sticking with 0.15% now. That dose seems to work best for me, and better the more often I use it.

Are you planning on buying more soon? I'm all out. What does .15% translate to in terms of mg?

 

[pegasus2]

Are you planning on buying more soon? I'm all out. What does .15% translate to in terms of mg?

Yes, I'm almost out. It's 1.5mg/ml. 3mg/day is what I do now. The latest patent on WIHN specifies application of shh agonist PWD 5-8.

 

[pegasus2]

https://www.freepatentsonline.com/20200197488.pdf

Epithelial Shh Leads to HF Neogenesis in Wounds.

To determine if Shh activation could induce HFN in scar-forming wounds, Shh was overexpressed in epithelial cells in K14-CreER; LSL-Shh or K14-CreER; LSL-Shh; Gli1-LacZ mice and HFN was examined in small wounds. To induce Shh overexpression, TAM was injected into control and K14-CreER; LSL-Shh or K14-CreER; LSL-Shh; Gli1-LacZ mice from PW1d to indicated time points in FIG. 24. This treatment resulted in extensive HFN in wounds compared to control wounds (FIG. 24a, b). Epidermal Shh overexpression resulted in Gli1 activation in both the epidermis and dermis, corresponding to the areas of HFN. Shh-driven hair germs expressed Lef1 and K17 and exhibited normal hair follicle morphogenesis. AP+ DPs were associated with overlying K17+ epithelial buds as typically observed in HFN. Eventually, many of these hair follicles (52±16%, mean±s.d.) grew downward to form mature hair follicles with hair shafts, an event rarely observed in control small wounds. New DP expressed Lef1 and Noggin as well as AP, further demonstrating their DP identity. Aberrant basaloid growths resembling superficial basal-cell carcinomas (BCCs) were rarely in these wounds.

Previous studies noted that HFN in large wounds in WT mice was limited to the central area of the wounds. Given the ability of Shh to induce ectopic HFN in small wounds, exogenous Shh might overcome the inability of new hair follicles to form outside this central region in large wounds. In large wounds from TAM-treated K14-CreER; LSL-Shh mice, extensive DP formation was observed covering the entire wound area compared with TAM-treated controls. (FIG. 24c-e). These results verify the potency of Shh activation to overcome regional inhibition of HFN.

Epithelial activation of Wnt and Shh signaling was previously identified as critical for hair regeneration; however, these same pathways may also induce skin epithelial cancers when experimentally or pharmacologically augmented. This basic study with preclinical mouse models shows that the capacity to create ectopic de novo DP in vivo by modulation of specific signals in the dermis may overcome this barrier and bring us closer to true skin renewal after injury.

It's important to note that they used a more potent form of SAG that we don't have access to:

Any SHH agonist known to one of skilled in the art can be used. Examples of Shh agonists include, but not limited to, Hh-Ag, Purmorphamine, SAG, and 20(S)-Hydroxycholesterol.

In a particular embodiment, the SHH agonist is Hh-Ag. Hh-Ag (also known as Hh-Ag1.5) is a small-molecule chemical agonist of Smoothened (Smo) receptor and is an activator of sonic hedgehog (Shh) signaling. It is derived from an initial synthetic hit compound “Hh-Ag1.1”, and optimized to achieve the activity IC50=1 nM for agonist activity.

SAG has an EC50 of 3nM.

FIG. 29. C57B6, wounded at P21, followed by subcutaneous injection of Hh-Ag from PWD5 to PWD8 increases hair follicle formation.

FIG. 30. Cultured human and mouse dermal cells treated with Shh agonist (i.e., Hh-Ag) showed increased hair follicle (HF) number, relative to control.

FIG. 34. Quantitation of recon assay of cultured mouse dermal cells treated with Shh Ag or infected with active Smo virus. Number of hair formed per assay was significantly higher in Shh agonist, Hh-Ag, treated cells, relative to control and Smo virus infected cells.

FIG. 36. Dose dependent response. High concentration of Hh-Ag inhibited HF formation.

 

[Sanchez1234]

I think that dose is too high. My results slowed down on higher doses too. I'm sticking with 0.15% now. That dose seems to work best for me, and better the more often I use it.

Photon does once every 3 weeks and you every day? Why the difference

 

[pegasus2]

Photon does once every 3 weeks and you every day? Why the difference

I don't do every day. I do either 4 days or 10 days at a time around wounding, then I stop until I wound again. I am thinking about doing every day though as past a certain point in wounding Wnts promote scarring instead of regeneration, but shh overcomes that. Using SAG every day takes away the timing uncertainty around that. Photon is using it once every 3 weeks because the less you activate hH signaling the safer it is. I doubt using it sparingly like that presents much risk.

 

[Photon]

I don't do every day. I do either 4 days or 10 days at a time around wounding, then I stop until I wound again. I am thinking about doing every day though as past a certain point in wounding Wnts promote scarring instead of regeneration, but shh overcomes that. Using SAG every day takes away the timing uncertainty around that. Photon is using it once every 3 weeks because the less you activate hH signaling the safer it is. I doubt using it sparingly like that presents much risk.

Please message me if you're ready to order and willing to do a group buy. I'll be doing it in lower doses and more frequent too.

 

[John Difool]

I tried Tretinoid and would never use it again on my hair.

 

[DavidsDome]

Using FedEx guarantees an inspection thru customs

Same happend to me with DHL. Customs informed the 'Meds agency' of my country and they sued my *** for importing meds over the border.
Package passed through DHL Leipzig. Be careful.

 

[John Difool]

DHL 100% customs inspection

 

[werefckd]

Interesting thread and it's nice that you guys are trying the stuff on yourselves. But the results gotten, if any, are a far cry from the cure for hair loss Christiano said it was, aren't they

You guys didn't get cancer either so that's the good part, skin cancer is no joke

 

[polishkickbuttowski]

Interesting thread and it's nice that you guys are trying the stuff on yourselves. But the results gotten, if any, are a far cry from the cure for hair loss Christiano said it was, aren't they

You guys didn't get cancer either so that's the good part, skin cancer is no joke

Have you seen pegasus' pics? Hes got really good results in a short amount of time and hes been bald for many years. For guys with less aggressive loss it could easily be a cure.

 

[werefckd]

Have you seen pegasus' pics? Hes got really good results in a short amount of time and hes been bald for many years. For guys with less aggressive loss it could easily be a cure.

I saw the pics and for me it was hard to tell. I took into consideration the feedback from the other users who tried it too. If the stuff was the real deal you bet the transformation pics would be all over the place. Love them for trying and sharing the results with us, true champs.

 

[ElToso]

Itraconazole, a commonly used anti-fungal that inhibits Hedgehog pathway activity and cancer growth

In a screen of drugs previously tested in humans we identified itraconazole, a systemic antifungal, as a potent antagonist of the Hedgehog (Hh) signaling pathway that acts by a mechanism distinct from its inhibitory effect on fungal sterol biosynthesis. ...

www.ncbi.nlm.nih.gov

mrOscar sent me this study. I'm reevaluating the use of ketoconazole.

 

[DavidsDome]

Itraconazole, a commonly used anti-fungal that inhibits Hedgehog pathway activity and cancer growth

In a screen of drugs previously tested in humans we identified itraconazole, a systemic antifungal, as a potent antagonist of the Hedgehog (Hh) signaling pathway that acts by a mechanism distinct from its inhibitory effect on fungal sterol biosynthesis. ...

www.ncbi.nlm.nih.gov

mrOscar sent me this study. I'm reevaluating the use of ketoconazole.

Inhibiting the HH pathway... this is the opposite of what we need, isnt it?

 

[Selb]

Honestly if the risk for sag and Hh agonist is cancer and you try it, you might as well go the nuclear route of CPA and huge doses of estrogen. And the hopefully taper off after hair regrowth and maintain with dutasteride and RU.

 

[John Difool]

Not unless you want to remain functioning as a male while you regain. Not everyone on hrt regrow hair.

 

[pegasus2]

Inhibiting the HH pathway... this is the opposite of what we need, isnt it?

That's why he's saying using keto shampoo might have a downside.

Honestly if the risk for sag and Hh agonist is cancer and you try it, you might as well go the nuclear route of CPA and huge doses of estrogen. And the hopefully taper off after hair regrowth and maintain with dutasteride and RU.

Pick your poison. Would you rather be bald, have cancer, or be a woman. The good thing for baldies is they are probably less likely to get cancer, aside from prostate cancer.

 

[Selb]

That's why he's saying using keto shampoo might have a downside.

Pick your poison. Would you rather be bald, have cancer, or be a woman. The good thing for baldies is they are probably less likely to get cancer, aside from prostate cancer.

Interesting since I figured keto 2% cream was an effective anti androgen. I was planning on using it so I wouldn’t have to jump on RU.

I can take feminizing myself for a year, maybe freezing sperm just in case, to try and regrow hair. And then hoping I can hop off it. But I guess I’m not desperate enough to actual do anything like that yet

 

[czecha]

Yeah but who tryna play with cancer.

Bunch of coritcosteroids are agonist for this
https://www.pnas.org/content/107/20/9323

@ChemHead @EndlessPossibilities
the corticosteroid you have been talking about in there by any chance? what do you think?


@everyone
do we know if finasteride upregulates any of those corticosteroids?

it was @ChemHead s theory that finasteride regrowth happens through upregulation of a corticosteroid. he has really informative posts here:

https://www.hairlosstalk.com/interact/threads/oral-steroid-made-my-hair-grow-back-thicker.106598/

maybe this is the same mechanism

One of the reasons why I strongly believe the steroid increased by finasteride may be a mineralocorticoid over a glucocorticoid is because mineralocorticoids regulate salt and fluid retention. When my hair gets thicker from finasteride, most of the thickening occurs in a pretty short time frame... I'm talking like inside of a week. It also transitions from thick to thin, dry, and falling out very rapidly... Like days. What could cause hair to increase and decrease in thickness that quickly? Surely, it can't be that the hair has created new proteins and then lost those proteins only days later. That wouldn't make sense. But what would make sense is that they swelled up due to fluid retention, from possibly a mineralocorticoid, and then rapidly deflated after that mineralocorticoid decreased back to it's normal deficient concentration. There's a lot of speculation on my part here, but everything I've discovered through experimentation currently leads me in this direction.

 

[Will Be an Egg in 5 years]

wtf we dont even understand hairloss yet

i'm tired of all this bullshit