jak in 5

JAK-IN-5 is a JAK inhibitor.

JAK-IN-5 hydrochloride is a JAK inhibitor [1].

SYK JAK-IN-1 is a dual SYK JAK inhibitor with IC50 values of less than 5 nM for both SYK and JAK2.

JAK-IN-20 is a potent, orally active, broad-based JAK inhibitor, effective on JAK1 (IC50: 7 nM), JAK2 (IC50: 5 nM), and JAK3 (IC50: 14 nM), exhibiting excellent pharmacokinetic and anti-inflammatory activity in vivo.

W1131, a potent STAT3 inhibitor, effectively triggers ferroptosis and suppresses cancer progression across various models including gastric cancer cell subcutaneous xenograft, organoids, and patient-derived xenograft (PDX). Additionally, W1131 overcomes chemical resistance in cancer cells to 5-FU by regulating cell cycle, DNA damage response, and oxidative phosphorylation pathways, notably the IL6-JAK-STAT3 and ferroptosis pathways [1].

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].

W1131 TFA is a potent STAT3 inhibitor inducing ferroptosis and effectively halting cancer progression in subcutaneous xenograft, organoid, and PDX models of gastric cancer. It mitigates chemoresistance to 5-FU in cancer cells and modulates the cell cycle, DNA damage response, and oxidative phosphorylation, targeting pathways such as IL6-JAK-STAT3 and ferroptosis [1].

ON044580 is an effective non-ATP-competitive inhibitor of JAK2, characterized as an α-benzoylstyrylbenzyl thioether. It exhibits IC50 values of 1.23 μM for wild type JAK2 and 1.09 μM for the V617F mutation. The compound inhibits JAK2 kinase activity by binding to the STAT-5 binding domain or the allosteric site of JAK2. In JAK2V617F-positive leukemia cells, ON044580 suppresses proliferation and induces apoptosis in Imatinib-resistant chronic myeloid leukemia (CML) cells. It also inhibits both wild type and T315I mutant forms of the BCR-ABL kinase. ON044580 is used in research for myeloproliferative diseases characterized by abnormal JAK STAT signaling.

JAK-IN-14 (compound 16) is a specific JAK1 inhibitor with IC50<5 μM. It prevents JAK1 phosphorylation by binding to the active site of JAK1, and is more than 8-fold selective for JAK1 over JAK2 JAK3, and can be used in immune, inflammation and cancer research.