target/TNF/2

Compound 5K (Multi-target kinase inhibitor 2) is a multi-targeted kinase inhibitor demonstrating activity against EGFR, Her2, VEGFR2, and CDK2 with IC50 values between 40 to 204 nM. It exhibits cytotoxic effects on HepG2, HeLa, MDA-MB-231, and MCF-7 cell lines, with IC50 values of 41, 57, 51, and 59 μM, respectively. Additionally, it induces cell cycle arrest and apoptosis specifically in HepG2 cells.

TAPI-2 is a broad-spectrum inhibitor of MMP (IC50: 20 μM), tumour necrosis factorα-converting enzyme (TACE) and a disintegrin and metalloproteinase (ADAM).

TNF-α-IN-2 is a highly potent and orally bioavailable inhibitor of tumor necrosis factor alpha (TNFα), exhibiting an IC50 of 25 nM in the HTRF assay. It exerts its inhibitory effects by inducing conformational changes in the TNFα trimer upon binding, resulting in disrupted signaling when the trimer interacts with TNFR1. TNF-α-IN-2 holds promise as a valuable tool for investigating the pathogenesis of rheumatoid arthritis[1].

Enavatuzumab (PDL192; ABT-361) is a humanized IgG1 monoclonal antibody designed to target the TWEAK receptor (TweakR), a protein involved in various cellular responses through its interaction with its natural ligand, TWEAK (Fn14; TNFRSF12A). By directly engaging TweakR signaling and promoting antibody-dependent cell-mediated cytotoxicity (ADCC), enavatuzumab effectively inhibits tumor growth. It also recruits and activates myeloid effector cells to destroy tumor cells. Enavatuzumab has demonstrated the ability to suppress the proliferation of a range of human TweakR-positive cancer cell lines and tumorigenic models both in vitro and in vivo [1] [2].