stat-5-in-1

STAT5-IN-1 (STAT5 Inhibitor) is a cell-permeable inhibitor which suppresses Stat5 via binding to the SH2 domain.

ζ-Stat (NSC37044), a specific and atypical inhibitor of PKC-ζ with an IC50 of 5 μM, demonstrates the ability to inhibit proliferation and induce apoptosis in melanoma cell lines, exhibiting antitumor activity in vitro[1][2].

Lipid-derived lipoxins are produced at the site of vascular and mucosal inflammation where they down-regulate polymorphonuclear leukocyte recruitment and function. 15(R)-Lipoxin A4 (15(R)-LXA4) is derived from the aspirin-triggered formation of 15(R)-HETE from arachidonic acid. [1] [2] 15(R)-LXA4 inhibits LTB4-induced chemotaxis, adherence, and transmigration of neutrophils with twice the potency of LXA4 demonstrating activity in the nM range.[2] [3] The anti-inflammatory effects of aspirin may be ascribed in part to the ability of 15(R)-LXA4 to regulate leukocyte function.[4] 15(R)-LXA4 is reported to promote resolution of inflammation in LPS-treated stromal cells derived from intermediate-stage diseased supraspinatus tendons as evidenced by increased expression of the STAT-6 pathway target genes, ALOX15 and CD206.[5]

HAT-SIL-TG-1&AT, a hypoxia-activated prodrug, functions as a Janus tyrosine kinase (JAK) inhibitor demonstrating antitumor effects by inhibiting JAK-STAT signaling within tumor tissues. It also suppresses the proliferation of HEL cells and downregulates phosphorylated STAT3 5 in hypoxic conditions.

5-epi-Arvestonate A, a sesquiterpenoid extracted from Seriphidium transiliense whole plants, enhances melanogenic production by stimulating MITF and tyrosinase family gene transcription. Additionally, it suppresses IFN-γ-chemokine expression via the JAK STAT signaling pathway in HaCaT cells [1].

3-O-Methylgallic acid (3,4-Dihydroxy-5-methoxybenzoic acid) reduces cell proliferation in Caco-2 cells (IC50 = 24.1 μM) more effectively than anthocyanins and may offer protection against colon cancer after its formation in the gut. It inhibits transcription factors NF-κB, AP-1, STAT-1, and OCT-1, which are known to be activated in colorectal cancer.