ANTI-HAIR LOSS 45 A
BINTERIN SYNEPIN
(EGF peptide)
- -
1µM -
1µM 0.1%
1µM 1%
B STAT3/POLII 14.00 10.50 7.00 3.50 0.00
_ _
1µM _
1µM 0.1%
1µM 1%
BINTERIN SYNEPIN
(EGF peptide)
Figure 4: Inhibitory effect of Jak1 inhibitor tripeptide on EGF tripeptide-induced STAT3–POL II interaction in human dermal papilla cells (DPCs). (A) Human DPCs were treated with an EGF-mimetic tripeptide, in the absence or presence of Jak1 inhibitor-Tripeptide (0.1% and 1%). The physical interaction between Signal Transducer and Activator of Transcription 3 (STAT3) and RNA Polymerase II (POL II) was visualized using an in situ proximity ligation assay (PLA). Red fluorescent puncta (rolling circle products, RCPs) represent individual STAT3/POL II complexes localized within the nuclei. Nuclei were counterstained with DAPI (blue). Original magnification, ×600. (B) Quantitative analysis of the PLA signals. The results are expressed as the average number of rolling circle products per cell (RCPs/cell). Data are presented as mean ± SD of three independent experiments
suppressor protein p53. MDM2, also as an E3 ubiquitin ligase, binds to P53, acts as a negative regulator of p53, primarily by targeting it for degradation and preventing its activation of genes that inhibit cell growth. MDM2 is often overexpressed in various cancers, and its ability to inhibit p53 contributes to uncontrolled cell proliferation. Protein phosphorylation is a major regulatory mechanism for cellular processes that determine growth, development, and death. Phosphorylation modulates protein activation, intracellular localization, expression, and degradation. In Western Blot and PLA Assays (Figure 5), Ac-
Tripeptide-4 Amide induces phosphorylation of p53 protein and activates p53 (P53-serin 15) while actin, a crucial protein involved in various cellular processes like muscle contraction, cytoskeletal
A BINTERIN 2% 5 15 30 60 min P53-pS15 MDM2
14 12 10 8 6 4 2 0
β-Actin Control BINTERIN
structure and scaffolding, and cell mobility remains unchanged. In PLA assay, the activated p53 is separated
from p53-MDM2 interaction and connected to RNA polymerase complex (P53-Pol II) and induces transcription of the target gene. The Rolling Circle Products (RCPs), long single stranded DNA molecules/products in P53-Pol II are dose- dependently increased. These results show that Ac-Tripeptide-4 Amide inhibits p53-MDM2 interaction and activates P53-Pol II.
AR inhibitor and Jak1 inhibitor combined tripeptides can suppress the DHT-induced expression of IL-6 that disrupts hair growth One of the most significant consequences of the DHT-AR binding in dermal papilla cells is the
B P53/MDM2 25 20 15 10 5 _ 0 0.1% 0.5% 1% 2% Control BINTERIN
Figure 5: Activation of p53 signaling by Ac-Tripeptide-4 Amide in human dermal papilla cells. (A) Human dermal papilla cells were treated with Jak1 inhibitor tripeptide (2%) for the indicated time points (5, 15, 30, and 60 min). Protein expression levels of phosphorylated p53 (p53-pS15) and MDM2 were analysed by Western blotting. β-Actin was used as a loading control. (B) Proximity ligation assay (PLA) was performed to evaluate p53/MDM2 and p53/POL II interactions in human dermal papilla cells treated with increasing concentrations of Jak1 inhibitor tripeptide. PLA signals were quantified and expressed as RCPs per cell. Data are presented as mean ± SD of three independent experiments
www.personalcaremagazine.com June 2026 PERSONAL CARE MAGAZINE _
upregulated secretion of Interleukin-6 (IL-6), a pro-inflammatory cytokine. The presence of elevated IL-6 leads to hair
loss. AR inhibitor tripeptide works as DHT pathway blocker. As shown in Figure 6, AR inhibitor tripeptide helps reduce genetic hair loss by inhibiting DHT pathway. On the other hand, Jak1 inhibitor tripeptide
can suppress the IL-6 induced inflammation as well, which can reduce hair loss.
AR Inhibitor tripeptide + Jak1 Inhibitor combined tripeptides can inhibit DHT-induced senescence (cell ageing) of dermal papilla cells DHT-induced senescence is a mechanism driving androgenetic alopecia and age-related tissue damage, where high DHT levels trigger
P53/POLII
0.1% 0.5%
1%
2%
Control
RCPs/Cell
RCPs/Cell
RCPs/Cell
Page 1 |
Page 2 |
Page 3 |
Page 4 |
Page 5 |
Page 6 |
Page 7 |
Page 8 |
Page 9 |
Page 10 |
Page 11 |
Page 12 |
Page 13 |
Page 14 |
Page 15 |
Page 16 |
Page 17 |
Page 18 |
Page 19 |
Page 20 |
Page 21 |
Page 22 |
Page 23 |
Page 24 |
Page 25 |
Page 26 |
Page 27 |
Page 28 |
Page 29 |
Page 30 |
Page 31 |
Page 32 |
Page 33 |
Page 34 |
Page 35 |
Page 36 |
Page 37 |
Page 38 |
Page 39 |
Page 40 |
Page 41 |
Page 42 |
Page 43 |
Page 44 |
Page 45 |
Page 46 |
Page 47 |
Page 48 |
Page 49 |
Page 50 |
Page 51 |
Page 52 |
Page 53 |
Page 54 |
Page 55 |
Page 56 |
Page 57 |
Page 58 |
Page 59 |
Page 60 |
Page 61 |
Page 62 |
Page 63 |
Page 64 |
Page 65 |
Page 66 |
Page 67 |
Page 68 |
Page 69 |
Page 70 |
Page 71 |
Page 72 |
Page 73 |
Page 74 |
Page 75 |
Page 76 |
Page 77 |
Page 78 |
Page 79 |
Page 80 |
Page 81 |
Page 82 |
Page 83 |
Page 84 |
Page 85 |
Page 86 |
Page 87 |
Page 88 |
Page 89 |
Page 90 |
Page 91 |
Page 92 |
Page 93 |
Page 94 |
Page 95 |
Page 96 |
Page 97 |
Page 98 |
Page 99 |
Page 100
