46 ANTI-HAIR LOSS DHT 100nM Control - 1.25%
ANDRIN +BINTERIN 2.5%
5.0%
IL-6
Figure 6: AR Inhibitor tripeptide + Jak1 Inhibitor tripeptides suppress DHT-induced IL-6 expression in human dermal papilla cells. Human dermal papilla cells (DPCs, HDC) were treated with DHT in the presence of increasing concentrations of AR Inhibitor tripeptide + Jak1 Inhibitor tripeptides under the indicated conditions. Immunofluorescence (IF) staining was performed to detect IL-6 (green), and nuclei were counterstained with DAPI (blue)
mitochondrial dysfunction, ROS accumulation, and premature senescence in dermal papilla cells (DPCs). This process stops cell growth and releases inflammatory factors, which can be inhibited by antioxidants. The Androgen Receptor (AR) plays a pivotal
role in the process of cell senescence induced by DHT. The DHT-AR complex acts as a central mediator that halts cell proliferation and induces a senescent phenotype by upregulating the expression of cell cycle inhibitors such as p53 and p21.
By the way, the protein-protein interaction
(PPI) between the tumour suppressor p53 and RNA polymerase II (Pol II) is a critical molecular mechanism where p53 regulates gene expression in response to cellular stress. This interaction allows p53, a transcription
factor, to directly influence the transcriptional machinery and modulate the transcription of target genes involved in cell cycle arrest, DNA repair, and apoptosis. In this interaction, Jak1 inhibitor tripeptide activates p53, which induces senescence of severely damaged zombie cells in
A DHT(20nM) Control - 1.25%
ANDRIN + BINTERIN 2.5%
dermal papilla cells (DPCs) and removes them. In fact, DHT drastically induces the senescence
of DPCs (Figure 7). However, treatment of DPCs with AR inhibitor tripeptide and Jak1 inhibitor tripeptide dose-dependently remove the senescence-induced damaged DPCs. Taken together, these results suggest that AR inhibitor tripeptide and Jak1 inhibitor tripeptide combination help prevent hair loss by not only reducing DHT-induced senescence of DPCs but also removing senescent cells.
Conclusion In conclusion, hair loss is caused by a complicated combination of several factors like genetics, hormonal shifts, medical conditions, and lifestyle factors. The most common cause is hereditary androgenetic alopecia (male/female pattern baldness). Other primary factors include stress, thyroid issues, nutritional deficiencies (vitamin D etc.), medications, autoimmune diseases (alopecia areata), and hair styling practices. So, two tripeptides, AR inhibitor tripeptide and Jak1 inhibitor tripeptide cannot solve all the hair
B 5.0%
250 200 150 100 50 0
Control _
loss issues completely, but, as tested in several in vitro and in situ assays like WB, PLA etc., are confirmed to help reduce at least two important hair loss factors like androgenic alopecia (AGA) caused by DHT and alopecia areata (AA) caused by autoimmune-issued inflammation. In addition, small molecule tripeptides like AR
inhibitor tripeptide and Jak1 inhibitor tripeptide are also known and proved to be safe, stable and topically applicable, which is a strong advantage as cosmetic ingredients. Actually, we have seen so many informal good case results when we topically applied both tripeptides alone or sometimes in combination of microneedling (MTS) for several hair loss patients for a couple of years. However, more scientific and multicentre
studies for larger numbers of hair loss subjects are still required. Also, we will be happy to collaborate with capable hair cosmetic labs for topical applications of the hair loss-preventing tripeptides. In addition to the hair loss-preventing tripeptides, Vitamin D receptor and AMPK agonist tripeptides will be available for hair regeneration soon.
PCM
1.25%
2.5%
5%
ANDRIN + BINTERIN DHT(20nM)
Figure 7: Inhibitory effect of AR inhibitor tripeptide and Jak1 inhibitor tripeptide on DHT-induced cellular senescence in human dermal papilla cells. (A) Human dermal papilla cells were treated with AR inhibitor tripeptide and Jak1 inhibitor tripeptide at the indicated concentrations (0.1%, 0.5%, 1%, and 2%). Cellular senescence was assessed by Senescence-associated β-galactosidase (SA-β-gal) staining. Representative images of SA-β-Gal-positive cells (green) are shown. (B) The percentage of SA-β-Gal-positive cells was quantified and expressed relative to the control. Data are presented as mean ± SD of three independent experiments
PERSONAL CARE MAGAZINE June 2026
www.personalcaremagazine.com
Senescent Cells (% of Control)
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