Is this company throwing away its hair growth treatment? It has been almost an entire year since their phase II was released, with somewhat disappointing results. Since then we have not heard a thing from them regarding their hair growth treatment. Anyone have any updates? I'm starting to think samumed's androgenetic alopecia trratment is dead.
Serious Question About Samumed And It's Viability
- Thread starter Pavi
- Start date
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- 8,251
It is not dead. They are going to share their findings soon in medical conferences .. and hopefully will start phase III.
Here is press release from end of Oct.
October 25, 2016 Samumed Successfully Completes a Phase II Androgenetic Alopecia (“Androgenetic Alopecia”) Biopsy Trial Studying Regeneration of Hair Follicles San Diego, CA – Samumed, LLC successfully completed a 135-day study of its topical compound, SM04554, on 49 male subjects with Androgenetic Alopecia analyzed by biopsy of the scalp prior to and post dosing. The safety and the efficacy results of this second Phase II Trial further support the safety and efficacy findings from the company’s prior trials. Moreover, the biopsy results support the program’s mechanism-of-action regarding new hair follicle regeneration. As the Company previously reported, efficacy data from its first Phase II Androgenetic Alopecia trial showed statistically significant increases for both objective outcome measures: non‐vellus hair count (a primary outcome measure) and hair density (a secondary outcome measure), using the pre‐specified statistical model. Further, in that first Phase II Androgenetic Alopecia study, there were no serious adverse events observed in any treated patient, and the incidence of adverse events was similar between treatment and vehicle groups. The Phase II Androgenetic Alopecia Biopsy study results will be presented at upcoming medical conferences.
https://www.samumed.com/medium/imag...biopsy-trial-studying-regenerati_35/view.aspx
Here is press release from end of Oct.
October 25, 2016 Samumed Successfully Completes a Phase II Androgenetic Alopecia (“Androgenetic Alopecia”) Biopsy Trial Studying Regeneration of Hair Follicles San Diego, CA – Samumed, LLC successfully completed a 135-day study of its topical compound, SM04554, on 49 male subjects with Androgenetic Alopecia analyzed by biopsy of the scalp prior to and post dosing. The safety and the efficacy results of this second Phase II Trial further support the safety and efficacy findings from the company’s prior trials. Moreover, the biopsy results support the program’s mechanism-of-action regarding new hair follicle regeneration. As the Company previously reported, efficacy data from its first Phase II Androgenetic Alopecia trial showed statistically significant increases for both objective outcome measures: non‐vellus hair count (a primary outcome measure) and hair density (a secondary outcome measure), using the pre‐specified statistical model. Further, in that first Phase II Androgenetic Alopecia study, there were no serious adverse events observed in any treated patient, and the incidence of adverse events was similar between treatment and vehicle groups. The Phase II Androgenetic Alopecia Biopsy study results will be presented at upcoming medical conferences.
https://www.samumed.com/medium/imag...biopsy-trial-studying-regenerati_35/view.aspx
- Reaction score
- 594
Judging from their phase 2 trial, at the doses they tried terminal hair count and density increases were almost negligible... It was just a 90 day trial though, and perhsps differ t doses may help more
what i think is that samumed is really a breakthrough treatment. just read the following study posted by another user @c_super2
http://medicalxpress.com/news/2016-12-embryonic-fate-skin-cells-sweaty.html very thankful to him because it just increased my faith in this treatment. also this makes their claim true about creating new hair follicles and one thing more we know baldness starts with increased sebum
which means those hair follicles turned into sweat gland because of increases activity of BMP.
so i think there should be a balance between BMP and WNT because WNT's as far as i know are responsible for hair follicle formation and BMP's for sweat gland.
Follistatin from Histogen's HSC blocks BPMs.
sumumed's molecule activates WNTs.
it was so easy
http://medicalxpress.com/news/2016-12-embryonic-fate-skin-cells-sweaty.html very thankful to him because it just increased my faith in this treatment. also this makes their claim true about creating new hair follicles and one thing more we know baldness starts with increased sebum
which means those hair follicles turned into sweat gland because of increases activity of BMP.
so i think there should be a balance between BMP and WNT because WNT's as far as i know are responsible for hair follicle formation and BMP's for sweat gland.
Follistatin from Histogen's HSC blocks BPMs.
sumumed's molecule activates WNTs.
it was so easy
- Reaction score
- 39
It's been said before but it's possible Samumed and follica will make an awesome combo. Because I wonder - is it enough to promote Wnt without first getting the cells into that embryonic state? Maybe even simple derma rolling + Samumed will yield awesome results.
Point is, this sh*t can't come out soon enough...
Point is, this sh*t can't come out soon enough...
Baldybald1
Established Member
- Reaction score
- 76
Who knows maybe it's one of the chemicals that follica wants to use
- Reaction score
- 950
Sebaceous glands and sweat glands are not the same thing.
Histogen already uses Wnt.
it was so easy
If only it was...
@InBeforeTheCure
i found this.
Blocking canonical Wnt signalling during skin development by expression of a dominant negative mutant transcription factor Lef1 (ΔNLef1) under the control of a keratin14 promoter results in transdifferentiation of hair follicle keratinocytes into mature sebocytes.15,16 De novo sebocyte differentiation occurs along the length of the hair follicle and is not defined to a particular region of the pilosebaceous unit.
here
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835892/
also it seems like SHH also play some contribution too, they should study SHH (Sonic Hedgehog).
now the thing is Histogen is just using Wnt7a along with growth factors and Follistatin.
on the other hand Samumed is using a molecule that activates wnt pathway. which i think will regulate all the wnt members because these are not only require to kick start the hair follicle generation but also maintaining its growth phase.
i found this.
Blocking canonical Wnt signalling during skin development by expression of a dominant negative mutant transcription factor Lef1 (ΔNLef1) under the control of a keratin14 promoter results in transdifferentiation of hair follicle keratinocytes into mature sebocytes.15,16 De novo sebocyte differentiation occurs along the length of the hair follicle and is not defined to a particular region of the pilosebaceous unit.
here
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835892/
also it seems like SHH also play some contribution too, they should study SHH (Sonic Hedgehog).
now the thing is Histogen is just using Wnt7a along with growth factors and Follistatin.
on the other hand Samumed is using a molecule that activates wnt pathway. which i think will regulate all the wnt members because these are not only require to kick start the hair follicle generation but also maintaining its growth phase.
- Reaction score
- 1,332
@InBeforeTheCure @Swoop
what you guys think about the fact that castration do not reverse the male pattern baldness but feminizing regime does.
what about if we agonize estrogen receptor in scalp it should.
what you guys think about the fact that castration do not reverse the male pattern baldness but feminizing regime does.
what about if we agonize estrogen receptor in scalp it should.
- Reaction score
- 636
I have the feeling we really need some stickie threads. It's frankly quite difficult to google together the know how hidden here.
It's quite obvious Ahmad's suggestions have been tested and declared failures, but i don't recall where exactly.
Wanting to educate Ahmad, I don't really know where to start. Same with myself tbh.
It's quite obvious Ahmad's suggestions have been tested and declared failures, but i don't recall where exactly.
Wanting to educate Ahmad, I don't really know where to start. Same with myself tbh.
- Reaction score
- 950
Yep, it's also been well-established that blocking canonical Wnt signaling in hair follicle stem cells (HFSCs) inhibits differentiation into commited HF progenitors and instead favors sebocyte differentiation.
I've asked this before, but I'll ask it again to see if anyone knows -- what is the actual mechanism of Samumed? Is it an actual Frizzled agonist (which I would consider a "true" Wnt agonist), or GSK3-beta inhibitor, or something else? I've searched for this but couldn't find anything.
Here's a list of genes upregulated by 17beta-estradiol (which is what those feminizing regimens use) in male hair follicles, which come from here; Supplementary Materials:
Code:
Gene Fold Change
FLNA 2.18
COMP 2.16
KRT19 1.92
KRT2 1.92
TAGLN 1.87
SRRM2 1.86
KRT75 1.85
LAMA5 1.76
PDLIM7 1.73
KRT37 1.73
KRT17 1.7
NKTR 1.64
MAGEA11 1.63
COL18A1 1.61
PMEL 1.57
ATP5D 1.56
ACTB 1.56
KRT14 1.55
COL6A2 1.54
CSPG4 1.54
MAP2K2 1.52
PTK7 1.52
GSTP1 1.52
CCND1 1.52
ERCC2 1.52
NFATC4 1.51
COL11A1 1.51
COL16A1 1.49
TKT 1.49
PPP1R13L 1.49
FOSL2 1.48
NDUFA3 1.47
KRT5 1.46
BASP1 1.44
MGP 1.43
EGFR 1.42And genes downregulated:
Code:
Gene Fold Change
MMP3 0.18
FLG 0.2
MMP1 0.32
SPP1 0.33
JAK1 0.35
FN1 0.36
ITGAV 0.37
SOD2 0.38
FGFR2 0.39
CDKN2B 0.4
GLRX 0.41
HACL1 0.41
AIM1 0.42
COL12A1 0.42
CDH1 0.43
CDKN1A 0.43
DCN 0.43
S100A9 0.44
SPRR2D 0.44
EPS8 0.44
HK2 0.45
CD36 0.45
S100A7 0.46
SPRR1A 0.46
SOCS5 0.46
NOV 0.47
LCN2 0.48
SPARCL1 0.48
MCL1 0.49
SDCBP 0.5
GJA1 0.5
TDG 0.5
CANX 0.5
CASP2 0.5
NID1 0.51
SERPINE1 0.51
IL1A 0.51
EDNRB 0.52
PTGDS 0.52
TNFRSF19 0.52
TXLNA 0.52
CCNG2 0.53
DSC1 0.53
ITGA6 0.53
CXCL1 0.53
IQGAP1 0.54
ITGB6 0.54
PDLIM5 0.54
MAPK14 0.54
DDX3X 0.55
EMP1 0.55
UBQLN1 0.56
TJP2 0.56
IL6 0.56
PLIN2 0.56
RAF1 0.56
EPS15 0.57
ITGA2 0.57
PPIL4 0.57
CALR 0.57
CCT8 0.57
EIF4H 0.58
ADAM9 0.58
ABCC5 0.58
MAPK6 0.59
SEC31A 0.59
HIF1A 0.6
GLUL 0.6
FOS 0.6
STAT2 0.6
STAT1 0.6
CCT4 0.6
FCGR1A 0.6
FMOD 0.61
VCAN 0.61
BCL2L13 0.62
COL6A3 0.62
THBS2 0.62
UNG 0.62
VEGFA 0.62
THBS1 0.62
LTBP1 0.62
ASAH1 0.62
GCLC 0.62
TNFRSF1A 0.62
CCNC 0.63
KRT38 0.63
MAPK1 0.63
CLU 0.63
IGFBP3 0.63
CD55 0.63
MCC 0.63
CASP8 0.63
HSPD1 0.64
S100A8 0.64
CORO1C 0.64
CDH5 0.64
TFDP1 0.64
DNAJA3 0.64
ERO1A 0.65
ABCB6 0.65
CD44 0.65
CGA 0.65
LUM 0.65
CDKN1B 0.65
PSAP 0.65
TGFA 0.65
CASP7 0.65
HADHB 0.65
GLIPR1 0.65
MFAP3 0.65
BCL10 0.65
PTK2 0.65
KRT1 0.65
CD34 0.66
ACOX1 0.66
VHL 0.67
EIF3E 0.67
BCL2L2 0.67
PSEN1 0.67
TNFSF10 0.67
LDLR 0.67
RIPK1 0.67
KRT36 0.67
PIM1 0.68
GJB2 0.68
B2M 0.68
LAMA4 0.68
XRCC5 0.68
CPE 0.68
HOPX 0.69
P4HB 0.69
PRKCH 0.69
LGALS8 0.69
MFAP5 0.69
VBP1 0.69
BCL2L1 0.69
ITGB1 0.7
CWC27 0.7
TP53 0.7
CTNNB1 0.7
MCM5 0.7
PDZK1IP1 0.7You can take the gene lists here and put them (without the corresponding fold changes) through gene ontology analysis here. Estrogen target genes are enriched for things like hair cycle, skin development, extracellular matrix remodeling, cytoskeletal dynamics and cell adhesion, cell migration, apoptosis, oxidative stress, cell proliferation, cell differentiation, inflammation, signaling pathways such as MAPK and NF-kB, and other things. How these all contribute to (sometimes miraculous) hair growth hasn't really been investigated, so we can only speculate.
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@hellouser you are using Lithium chloride which is a wnt agonist why don't you try to add follistatin? That way will have more stem cell to turn in to hair follicles.
- Reaction score
- 2,634
Point me to a source where I can buy it and I'll think about it.
- Reaction score
- 2,634
Dear god, that is not cheap, lol.