Peptide R54 acetate

Peptide R54 acetate (Pep R54 acetate) is a CXCR4 antagonist. Peptide R54 acetate inhibits CXCL12 -dependent activation of pERK1/2 and pAKT. The combination of Peptide R54 acetate and Nivolumab suppresses melanoma growth. Peptide R54 (acetate) is applicable to research related to melanoma and ovarian cancer ^{[1] [2]}.

In Vivo, Combination treatment with Peptide R54 (2 mg/kg; i.p.; 5 days per week for 3 consecutive weeks) acetate and Nivolumab significantly inhibits the growth of PES43 melanoma xenografts^[1].

In Vitro, Peptide R54 (100 nM; 16 h) acetate significantly inhibits CXCR4-dependent migration toward CXCL12 and CXCL11 in CAOV3, OVCAR8 and IGROV1 ovarian cancer cells^[2]. Peptide R54 (100 nM; 24 h) acetate inhibits CXCR4-mediated mesenchymal transition by restoring the expression levels of EMT markers in CAOV3, OVCAR8 and IGROV1 ovarian cancer cells^[2]. Peptide R54 (100 nM; 10 min) acetate inhibits CXCR4 downstream signaling pathways by reversing CXCL12-induced phosphorylation of ERK1/2, AKT and p38, as well as reversing the upregulation of RAC1 in CAOV3, OVCAR8 and IGROV1 ovarian cancer cells^[2]. Peptide R54 (100 nM; 24-72 h) acetate attenuates CXCL12-induced proliferation and sensitizes CAOV3, OVCAR8 and IGROV1 ovarian cancer cells to cisplatin and paclitaxel^[2].

References:
[1]. D'Alterio C, et al. Targeting CXCR4 potentiates anti-PD-1 efficacy modifying the tumor microenvironment and inhibiting neoplastic PD-1. J Exp Clin Cancer Res. 2019;38(1):432. Published 2019 Oct 28.
[2]. Russo D, et al. The CXCR4 antagonist R54 targets epithelial-mesenchymal transition (EMT) in human ovarian cancer cells. PLoS One. 2024;19(12):e0314735. Published 2024 Dec 19.