- Reaction score
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i asked Her When will the clinical trials For HMI-115 start and in which country. Also the question When they Plan to commercialize and When will they give an Update to the Public
Bayer Prolactin Receptor Antibody For Male And Female Pattern Hair Loss
- Thread starter Ollie
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i asked Her When will the clinical trials For HMI-115 start and in which country. Also the question When they Plan to commercialize and When will they give an Update to the Public
Let's hope she replies with something more than before.
- Reaction score
- 984
Dear Sender,
Thank you for your email.
I am on my annual leave at the moment with limited access to email.
You may reach me at WeChat or calling +86 18301852397. I'll get back to you as soon as I can. Thanks for your understanding!
Best Regards,
Amber Chen 陈婧
Senior Manager, Admin and Corporate Affairs
Room 306, Building Y1, Liangxiu Road, Pudong New Area, Shanghai, China
上海市浦东新区亮秀路112号Y1座306
Mobile: +86 18301852397
Phone: +86 21-5029-2097
amber.chen@hopemedinc.com<mailto:amber.chen@hopemedinc.com>
—-
So now the task is getting him on WeChat
Thank you for your email.
I am on my annual leave at the moment with limited access to email.
You may reach me at WeChat or calling +86 18301852397. I'll get back to you as soon as I can. Thanks for your understanding!
Best Regards,
Amber Chen 陈婧
Senior Manager, Admin and Corporate Affairs
Room 306, Building Y1, Liangxiu Road, Pudong New Area, Shanghai, China
上海市浦东新区亮秀路112号Y1座306
Mobile: +86 18301852397
Phone: +86 21-5029-2097
amber.chen@hopemedinc.com<mailto:amber.chen@hopemedinc.com>
—-
So now the task is getting him on WeChat
- Reaction score
- 977
This paper is from 1994
"Recent studies have shown that there are two isoenzymes
of 5a-reductase in rats and humans (16, 17). Human scalp
skin expresses human 5a-reductase-1 at relatively high levels
(18). Characterization of the 5a-reductase activity displayed
in stumptail macaque skin has not been possible due to the
very low levels of enzyme activity in scalp (9) and the
unavailability of sufficient tissue for analysis"
It is so with recent investigations?
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- 984
Is anybody able to contact him in WeChat?
Please don't bother these people on vacation
The source for that is not available online. Due to the "unavailability of sufficient tissue" it is not possible to say if there is more or less 5-ar than in humans. I think the point is moot, as whether they have less 5-ar and more sensitive androgen receptors or vice versa, the process is the same, AR activation causes baldness.
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Posting this human study again for the people who have forgotten about it or never read the whole thread. Some Canadians claim that experimenting with sulforaphane(broccoli sprouts) is more scientifically valid than PRLR antagonists, but there is zero indication in the scientific literature that sulforaphane or NRF2 is responsible for the pattern of hair loss found in Androgenetic Alopecia. There is for prolactin. That's not to say that NRF2 activation isn't helpful, but it is not a lack of NRF2 activation that causes Androgenetic Alopecia so it cannot cure it.
"PRL represents a promising candidate gene for the hair growth defects observed in Androgenetic Alopecia-affected HFs. Moreover, PRL stimulates adrenal androgen production and elevated PRL levels have been reported to be accompanied by hirsutism and hair loss from the scalp, which resembles the pattern observed in Androgenetic Alopecia.[74-76] Also notable in the context of Androgenetic Alopecia is the observation of sex- and location-dependent hair growth regulatory effects for PRL in studies of human ex vivo HFs. While PRL promoted hair growth/hair shaft elongation in HFs derived from female frontotemporal scalp, PRL treatment of isolated male occipital scalp HFs resulted in premature catagen induction and thus the inhibition of hair growth.[77] This observation has been further substantiated on a molecular level, since PRL treatment resulted in sex‐ and site‐specific differences in gene expression.[77] Furthermore, analyses of plucked HFs from male frontal and occipital scalp revealed differential expression for several microRNAs (miRNAs) that target PRL signalling.[64] Together, these findings suggest that PRL action may contribute to the observed differences in Androgenetic Alopecia susceptibility between frontal and occipital HFs and the resulting characteristic hair loss pattern"
onlinelibrary.wiley.com
While I think that broccoli sprouts are too weak to be of any use, I do think more potent NRF2 activators are worthwhile. It improves both hair and skin. I posted this patent last year for oltipraz:
"Fibroblast population in the dermis of the Oltipraz treated group was significantly higher than that of the control and vehicle groups. Fibroblast population in Oltipraz treated group was reported 92.29% higher than the controls (p=0.003) and 104.25% higher than the vehicle group (p=0.003).The volume density of the collagen bundles was 38.03% and 57.75% higher in the oltipraz treated group compared to the control and the vehicle groups, respectively, which both were statistically significant (p<0.001). Consequently, the volume density of hair follicles was higher in the oltipraz group in comparison to the control (66.1%; P=0.043) and the vehicle (210%; p=0.001) groups"
https://patents.google.com/patent/KR101165648B1/en
I think it's more useful for hair pigmentation than hair growth, but it should help both.
"PRL represents a promising candidate gene for the hair growth defects observed in Androgenetic Alopecia-affected HFs. Moreover, PRL stimulates adrenal androgen production and elevated PRL levels have been reported to be accompanied by hirsutism and hair loss from the scalp, which resembles the pattern observed in Androgenetic Alopecia.[74-76] Also notable in the context of Androgenetic Alopecia is the observation of sex- and location-dependent hair growth regulatory effects for PRL in studies of human ex vivo HFs. While PRL promoted hair growth/hair shaft elongation in HFs derived from female frontotemporal scalp, PRL treatment of isolated male occipital scalp HFs resulted in premature catagen induction and thus the inhibition of hair growth.[77] This observation has been further substantiated on a molecular level, since PRL treatment resulted in sex‐ and site‐specific differences in gene expression.[77] Furthermore, analyses of plucked HFs from male frontal and occipital scalp revealed differential expression for several microRNAs (miRNAs) that target PRL signalling.[64] Together, these findings suggest that PRL action may contribute to the observed differences in Androgenetic Alopecia susceptibility between frontal and occipital HFs and the resulting characteristic hair loss pattern"
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While I think that broccoli sprouts are too weak to be of any use, I do think more potent NRF2 activators are worthwhile. It improves both hair and skin. I posted this patent last year for oltipraz:
"Fibroblast population in the dermis of the Oltipraz treated group was significantly higher than that of the control and vehicle groups. Fibroblast population in Oltipraz treated group was reported 92.29% higher than the controls (p=0.003) and 104.25% higher than the vehicle group (p=0.003).The volume density of the collagen bundles was 38.03% and 57.75% higher in the oltipraz treated group compared to the control and the vehicle groups, respectively, which both were statistically significant (p<0.001). Consequently, the volume density of hair follicles was higher in the oltipraz group in comparison to the control (66.1%; P=0.043) and the vehicle (210%; p=0.001) groups"
https://patents.google.com/patent/KR101165648B1/en
I think it's more useful for hair pigmentation than hair growth, but it should help both.
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- Reaction score
- 977
Thank you.
"the stumptail macaque {Macaca speciosa) develops frontal hair thinning after puberty. The process starts around age 3 yr, is well advanced by age 6 yr, and occurs to an equal degree in both sexes (3-5). Balding does not occur in castrated monkeys, but it can be induced by treating the castrated animals with T (6). The balding process in stumptail macaques is characterized by a gradual conversion of terminal follicles to vellus follicles (4). Biochemically, skin from the frontal scalp of these monkeys metabolizes T at a greater rate than does skin from the occipital scalp (7). Hence, both histological changes and androgen metabolism in the scalp of the balding stumptail macaque are similar to those found in human male-pattern baldness."
" The three treated monkeys had no signs of baldness clinically or anatomically, while two of the three
control monkeys had marked balding changes. The third control monkey (no. 4) also had the early development
of baldness, which did not progress further, probably because of incomplete pubertal development. Although
his serum androgen levels were in the female range for most of the study, he had less baldness than the control
female (no. 6). His skin 5a-reductase level was only 40% that of the control female, suggesting that diminished
production of DHT in the scalp might be responsible for the delayed balding process."
Clearly PRLR inhibition reverses androgen-induced hair loss. There's no guarantee that there isn't some compensatory mechanism in humans that is not present in macaques which will make up for the loss of PRLR signalling, but this is the most promising treatment we've ever had in trials by far.
- Reaction score
- 977
Different from humans????
Humans have longer lifespans, macaques hit puberty at 3 years old. It is more aggressive than in humans, as most humans don't start balding until later in life. Macaques probably have more AR expression or are less resistant to cellular stress so they start balding immediately upon increased DHT production.
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- 340
I see Oltipraz is used to prevent cancer, but as soon as something is in some way related to cancer, I have to ask, is there any concern that it might have a pro-cancer effect if used excessively or for any other reason?Posting this human study again for the people who have forgotten about it or never read the whole thread. Some Canadians claim that experimenting with sulforaphane(broccoli sprouts) is more scientifically valid than PRLR antagonists, but there is zero indication in the scientific literature that sulforaphane or NRF2 is responsible for the pattern of hair loss found in Androgenetic Alopecia. There is for prolactin. That's not to say that NRF2 activation isn't helpful, but it is not a lack of NRF2 activation that causes Androgenetic Alopecia so it cannot cure it.
"PRL represents a promising candidate gene for the hair growth defects observed in Androgenetic Alopecia-affected HFs. Moreover, PRL stimulates adrenal androgen production and elevated PRL levels have been reported to be accompanied by hirsutism and hair loss from the scalp, which resembles the pattern observed in Androgenetic Alopecia.[74-76] Also notable in the context of Androgenetic Alopecia is the observation of sex- and location-dependent hair growth regulatory effects for PRL in studies of human ex vivo HFs. While PRL promoted hair growth/hair shaft elongation in HFs derived from female frontotemporal scalp, PRL treatment of isolated male occipital scalp HFs resulted in premature catagen induction and thus the inhibition of hair growth.[77] This observation has been further substantiated on a molecular level, since PRL treatment resulted in sex‐ and site‐specific differences in gene expression.[77] Furthermore, analyses of plucked HFs from male frontal and occipital scalp revealed differential expression for several microRNAs (miRNAs) that target PRL signalling.[64] Together, these findings suggest that PRL action may contribute to the observed differences in Androgenetic Alopecia susceptibility between frontal and occipital HFs and the resulting characteristic hair loss pattern"
Error - Cookies Turned Off
While I think that broccoli sprouts are too weak to be of any use, I do think more potent NRF2 activators are worthwhile. It improves both hair and skin. I posted this patent last year for oltipraz:
"Fibroblast population in the dermis of the Oltipraz treated group was significantly higher than that of the control and vehicle groups. Fibroblast population in Oltipraz treated group was reported 92.29% higher than the controls (p=0.003) and 104.25% higher than the vehicle group (p=0.003).The volume density of the collagen bundles was 38.03% and 57.75% higher in the oltipraz treated group compared to the control and the vehicle groups, respectively, which both were statistically significant (p<0.001). Consequently, the volume density of hair follicles was higher in the oltipraz group in comparison to the control (66.1%; P=0.043) and the vehicle (210%; p=0.001) groups"
https://patents.google.com/patent/KR101165648B1/en
I think it's more useful for hair pigmentation than hair growth, but it should help both.
- Reaction score
- 453
So, it's over?
- Reaction score
- 984
Yes it is. Unfortunately they didnt reach their goal to start trials in 2021. the Next Huge disappointment. They Aren‘t able to communicate their problems. They failed so hard
HMI-115 was the Last Chance i was hoping For…
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How is it possible that oltipraz is an inhibitor of hif1a when it is known that it activates cell proliferation in hypoxia, damn it's really hard to look for a square in this pathologyPosting this human study again for the people who have forgotten about it or never read the whole thread. Some Canadians claim that experimenting with sulforaphane(broccoli sprouts) is more scientifically valid than PRLR antagonists, but there is zero indication in the scientific literature that sulforaphane or NRF2 is responsible for the pattern of hair loss found in Androgenetic Alopecia. There is for prolactin. That's not to say that NRF2 activation isn't helpful, but it is not a lack of NRF2 activation that causes Androgenetic Alopecia so it cannot cure it.
"PRL represents a promising candidate gene for the hair growth defects observed in Androgenetic Alopecia-affected HFs. Moreover, PRL stimulates adrenal androgen production and elevated PRL levels have been reported to be accompanied by hirsutism and hair loss from the scalp, which resembles the pattern observed in Androgenetic Alopecia.[74-76] Also notable in the context of Androgenetic Alopecia is the observation of sex- and location-dependent hair growth regulatory effects for PRL in studies of human ex vivo HFs. While PRL promoted hair growth/hair shaft elongation in HFs derived from female frontotemporal scalp, PRL treatment of isolated male occipital scalp HFs resulted in premature catagen induction and thus the inhibition of hair growth.[77] This observation has been further substantiated on a molecular level, since PRL treatment resulted in sex‐ and site‐specific differences in gene expression.[77] Furthermore, analyses of plucked HFs from male frontal and occipital scalp revealed differential expression for several microRNAs (miRNAs) that target PRL signalling.[64] Together, these findings suggest that PRL action may contribute to the observed differences in Androgenetic Alopecia susceptibility between frontal and occipital HFs and the resulting characteristic hair loss pattern"
Error - Cookies Turned Off
While I think that broccoli sprouts are too weak to be of any use, I do think more potent NRF2 activators are worthwhile. It improves both hair and skin. I posted this patent last year for oltipraz:
"Fibroblast population in the dermis of the Oltipraz treated group was significantly higher than that of the control and vehicle groups. Fibroblast population in Oltipraz treated group was reported 92.29% higher than the controls (p=0.003) and 104.25% higher than the vehicle group (p=0.003).The volume density of the collagen bundles was 38.03% and 57.75% higher in the oltipraz treated group compared to the control and the vehicle groups, respectively, which both were statistically significant (p<0.001). Consequently, the volume density of hair follicles was higher in the oltipraz group in comparison to the control (66.1%; P=0.043) and the vehicle (210%; p=0.001) groups"
https://patents.google.com/patent/KR101165648B1/en
I think it's more useful for hair pigmentation than hair growth, but it should help both.
on the other hand, on prolactin, is it established that there is a direct relationship with androgens or does it act through other common pathways with androgens?
if the first we are still screwed, you can not mess with androgens
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- 146
Sorry, how is it over?