44 ANTI-HAIR LOSS A DHT(20nM) Control - 0.1%
ANDRIN 0.1%
B AR/POLII 10%
350 300 250 200 150 100 50 0
Control _ 0.1% 1% ANDRIN DHT(20nM)
Figure 2: Effect of Tripeptide-80 on DHT-induced AR–POL II interaction in LNCaP cells. (A) LNCaP cells were treated with DHT (20 nM) in the presence of AR inhibitor tripeptide (0.1%, 1%, 10%) for the indicated time. The interaction between androgen receptor (AR) and RNA polymerase II (POL II) was evaluated using an in situ proximity ligation assay (PLA). Red fluorescent puncta (rolling circle products, RCPs) indicate individual AR/POL II complexes, and nuclei were counterstained with DAPI (blue). Magnification, ×600. (B) PLA signals were quantified and expressed as rolling circle products per cell (RCPs/cell)
When treated with AR inhibitor tripeptide, the
DHT-induced interaction of AR (androgen receptor) and POL II are also dose-dependently inhibited, showing that AR inhibitor tripeptide inhibits DHT- induced AR-POLII interaction (Figure 2). In situ proximity ligation assay (PLA) (Figure
1) is a highly sensitive, antibody-based imaging technique used to detect, visualize and quantify endogenous protein-protein interactions, modifications, and localization within cells or tissue sections. In the context of LNCaP cells, AR-POL II refers
to androgen receptor (AR) and RNA polymerase II (Pol II), a crucial interaction in gene regulation. AR is a transcription factor that regulates gene expression in response to androgens, while Pol II is the enzyme responsible for transcribing DNA into mRNA. Their interaction is essential for androgen-driven gene expression. When LNCaP cells are treated with AR inhibitor
tripeptide, the expression of prostate antigen is dose-dependently reduced (Figure 3). This result shows that AR inhibitor tripeptide reduces DHT- induced PSA (prostate specific antigen) expression by inhibiting DHT-induced AR activity. The key function of the AR inhibitor tripeptide
is preventing androgen receptor (AR) from binding to specific DNA sequences to control gene expression and promotes follicular revitalization.
Jak1 Inhibitor tripeptide inhibits JAK-STAT activation that induces hair loss Alopecia areata (AA) is a common autoimmune disease characterized by non-scarring hair loss ranging from patches on the scalp to complete hair loss involving the entire body. The good efficacy from large-scale clinical trials of the JAK inhibitor Baricitinib made the first-in-disease FDA-approved treatment available for AA in June of 2022.
The JAK-STAT pathway is a rapid signaling
cascade used by cells to transmit information from extracellular cytokine receptors to the nucleus, directly regulating gene expression for proliferation, differentiation, and immune
PERSONAL CARE MAGAZINE June 2026 DHT(20nM) - 0.1%
ANDRIN 0.1%
10% PSA 10%
β-Actin
Figure 3: Effect of AR inhibitor tripeptide on DHT-induced PSA expression in LNCaP cells. LNCaP cells were treated with DHT (20 nM) in the presence of Tripeptide-80 (0.1%, 1%, 10%) for the indicated time. Protein expression levels of prostate-specific antigen (PSA) were analysed by Western blotting. β-Actin was used as a loading control
response. It consists of Janus kinases (JAKs) and signal transducers and activators of transcription (STATs). In dermal papilla cells, JAK-STAT pathway is
being explored as a potential target for treating hair loss conditions, such as alopecia areata and androgenetic alopecia. When JAK-STAT pathway is activated too much, immune system is being attacked and induces inflammatory responses, causing alopecia areata. And also increased expression of STAT3 genes is reported to cause androgenic alopecia. In the PLA assay (Figure 4), Ac-Tripeptide-4
Amide dose-dependently inhibits JAK-STAT signaling pathway, which can help to reduce the hair loss.
Jak1 inhibitor tripeptide activates p53 that induces senolytic effects Because senescent cells often have a higher ‘primed’ level of pro-survival signaling, stabilizing p53 through MDM2 inhibition can tip the balance toward apoptosis. While p53 is traditionally
known for inducing senescence, modern research has identified a senolytic effect—the ability to selectively kill existing senescent cells—by manipulating its activity or its interaction with specific “survival” proteins. In senescent cells, p53 often exists in a
‘tethered’ or inhibited state that prevents it from triggering apoptosis. Releasing this inhibition allows p53 to transition from a promoter of cell- cycle arrest to an executioner of cell death. p53, also known as tumour protein p53 or
TP53, is a crucial tumour suppressor protein that plays a vital role in regulating cell division and preventing cancer development. It acts as a transcription factor and controls the expression of other genes involved in various cellular processes like DNA repair, cell cycle arrest, and programmed cell death (apoptosis). p53 is often referred to as the ‘guardian of the genome’, due to its ability to protect cells from damage and maintain genomic stability.
MDM2 (Mouse double minute 2) is a protein that plays a crucial role in regulating the tumour
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Control
RCPs/Cell
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