You're afraid of inhibiting prolactin, but you are comfortable injecting osteopontin?
By the way, don't expect much regrowth from osteopontin. Estradiol inhibits osteopontin significantly. HMI-115 is certainly better.
HMI-115 PRLR antibody: The Most Promising Treatment Ever
- Thread starter pegasus2
- Start date
I have never talked about osteoporina
Amplifica is osteopontin. Unless you meant their second program, SCUBE3, which is also unlikely to work well.
SCUBE3 is downstream of highly oncogenic Shh activation. On the surface it should be assumed riskier than HMI-115.
SCUBE3 serves as an independent poor prognostic factor in breast cancer - PMC
Accumulating evidences indicate that the signal peptide-CUB-EGF-like domain-containing protein 3 (SCUBE3) plays a key role in the development and progression of many human cancers. However, the underlying mechanism and prognosis value of SCUBE3 in ...
www.ncbi.nlm.nih.gov
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Any news on the next phase?
Because unless you are an hyper-responder you wont get enough regrowth with that. Most people here need to recover a couple of NWs. And with RU you are not degrading the receptor, just blocking it.
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With how feverishly debated AR inhibitors are in terms of either real or illusory effects on the body, I'm shocked that there isn't more hesitancy or skepticism of HMI-115 by those same impassioned individuals. Especially given that there's no "just stop taking it" option with this type of administration, alongside the fact that abnormal prolactin levels at least has some relationship with both sexual function, brain function, and metabolic function in men.
It seems like there's every reason for people who are afraid of finasteride/dutasteride/RU to be more afraid of this.
It seems like there's every reason for people who are afraid of finasteride/dutasteride/RU to be more afraid of this.
So far the evidence is that it's completely safe. It seems to increase libido, whereas oral AR antagonists always decrease it. If Moe's results hold true, and everyone is able to maintain on PRLR inhibition, then it is superior to anti-androgens. It doesn't make sense to be concerned about bad studies showing correlations and possible connections to sexual dysfunction, when anti-androgens are confirmed to be causative in sexual dysfunction in humans.
This is already posted on the first page, but I'll repost for the people who don't read.
All known adverse effects of prolactin are caused by overproduction.
No side effects in monkeys. No side effects in human trials thus far. No known adverse effects from low low prolactin production in humans. No research in animals showing any causative negative effect of low prolactin on sexual, brain or metabolic function. The biggest side effects from HMI are likely to be increased libido, and reduced risk of cancer.
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That's the issue. Since very little is known about the effects of low prolactin levels other than no apparent adverse effects, it empowers any made up side effects people theorize based on tangential relationships they find in studies. Seems like an even easier landscape to farm fear and doubt than the past 40 years of AR inhibitors. The semi-permanence alone seems like it might scare people off more than AR inhibitors.
We can't even rely on animal models to predict how HMI's primary intended effects will transfer over to humans. The lack of (documented) side effects in animals is only moderately instructive here.
The cabergoline example is the main reason why I think HMI won't be taken down by side effect problems. That drug has been around for decades.
But anything that affects hormones will produce a small percentage of people who get heavily (and sometimes unpredictably) affected by it. It will probably happen with HMI too.
The cabergoline example is the main reason why I think HMI won't be taken down by side effect problems. That drug has been around for decades.
But anything that affects hormones will produce a small percentage of people who get heavily (and sometimes unpredictably) affected by it. It will probably happen with HMI too.
There have now been 3 human trials, and research shows that low prolactin does not cause problems in humans. I think people are looking for magic rather than drugs. Your going to be very lucky to find a drug with less tradeoffs than HMI-115. If you can't accept any tradeoffs then you don't really want hair. I can't understand why people think they should have their cake and eat it too with zero risk of even the slightest side effect. Spoiled brats. Nothing is ever good enough for this generation.
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Phase 2 started in September in China
folliclethought.com
HMI-115 Begins Phase 2 Trial In China – Follicle Thought
folliclethought.com
- 180 male participants will enter the study.
- 24 week / 6 month treatment period for all participants.
- The phase 2 trial began September 2023 and is expected to complete by December 2024.
- The trial is randomized, multicenter, double-blind, and placebo-controlled.
- Primary outcome is the mean change in target area hair count (TAHC) of non-vellus hairs from baseline.
- Norwood scales 3 vertex, 4, and 5 will be accepted to participate.
- Four cohorts will be formed, including a placebo group, and three groups receiving HMI-115 injections of either 120mg once every four weeks, 240mg once every four weeks, or 240mg once every two weeks.
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The safety trial was 240mg once every 2 weeks.
So for anyone thinking that they were going to increase the dosage for phase 2 trials and be more effective, for the phase 2 trial they're doing another group of 240mg/2weeks again and then 2 more groups of lower dosage, 120mg/4weeks and 240mg/4weeks.
It is funny though how every new almost-treatment still dance around the same few mechanisms whose correlations have been known about for 40 years. Maybe AI will be able to look through every old study and make these connections better and faster than people can.
So for anyone thinking that they were going to increase the dosage for phase 2 trials and be more effective, for the phase 2 trial they're doing another group of 240mg/2weeks again and then 2 more groups of lower dosage, 120mg/4weeks and 240mg/4weeks.
It is funny though how every new almost-treatment still dance around the same few mechanisms whose correlations have been known about for 40 years. Maybe AI will be able to look through every old study and make these connections better and faster than people can.
It's actually been known for months what the dosages would be in the phase II. They announced it long ago.
AI is going to need to get a lot better before it's better than humans at target prediction. Maybe in another 15 years, but by that time we will be cured already. Hair cloning is already a reality.
AI is going to need to get a lot better before it's better than humans at target prediction. Maybe in another 15 years, but by that time we will be cured already. Hair cloning is already a reality.
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I don't consider transplanting even an infinite supply of healthy follicles a cure. It's close to one, but it's still not your natural follicle arrangement. A cure would be the complete revitalization of all your existing miniaturized follicles back to their state before the effects of Androgenetic Alopecia. Would much rather have my natural hair than some doctor's arrangement of follicles. Though I can see it becoming a cosmetic gimmick for even people that aren't suffering from Androgenetic Alopecia if the tech reaches a point where they can control stuff like melanocyte activity in the transplanted follicles.
There has been a lot of progress in tangential fields like organ cloning, but given how there has been little to no progress over the past 15 years in terms of understanding Androgenetic Alopecia, I don't expect much of a difference over the next 15 on that front.
There has been a lot of progress in tangential fields like organ cloning, but given how there has been little to no progress over the past 15 years in terms of understanding Androgenetic Alopecia, I don't expect much of a difference over the next 15 on that front.
If you want to split hairs then ok, but it meets the strict sense of the definition for the word cure. Hair cloning is as close to a cure as you can ask for. The hair germs when implanted will connect to the APM automatically which controls direction, so flow of the hair will be just like your natural hair. They can increase the size of the hair shaft on the crown, and reduce it on the front and sides to make that match your natural hair too. Melonocyte activity etc., is all coded in your genes. With the method Tsuji uses the hair color and texture will be almost identical to your natural hair.
There has been massive progress in both understating Androgenetic Alopecia and in hair cloning in the last 15 years. It's impossible to overstate how much progress has been made. We didn't know anything 15 years ago.
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Phase 2 results will be considered a "now or never" situation for HMI 115? Should we keep our expectations low?