SPD304 dihydrochloride is a selective TNF-α inhibitor, which promotes dissociation of TNF trimers and therefore blocks the interaction of TNF and its receptor. SPD304 has an IC₅₀ of 22 µM for inhibiting in vitro TNF receptor 1 (TNFR1) binding to TNF-α.

SPD304 (2 μM) significantly rescues the survivability of aHSCs, reduces the production of lipid hydroxides, and increased intracellular GSH. The co-treatment of GA (75 μM) and SPD304 (2 μM), down-regulate TRADD almost 2-fold (w/o inhibitor vs. w/ inhibitor) and p−RIP3 1.4−fold compared to GA alone, and promotes caspase 8 activation^[4].

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

SPD304 cannot be used in vivo due to its high toxicity.

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

SPD304 cannot be used in vivo due to its high toxicity.

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

• . Molly M. He, et al. Small-Molecule Inhibition of TNF-α. Science 11 Nov 2005.

  . Alexiou P, et al. Rationally designed less toxic SPD-304 analogs and preliminary evaluation of their TNF inhibitory effects. Arch Pharm (Weinheim). 2014 Nov;347(11):798-805.  [Content Brief]

  . Mouhsine H, et al. Identification of an in vivo orally active dual-binding protein-protein interaction inhibitor targeting TNFα through combined in silico/in vitro/in vivo screening. Sci Rep. 2017 Jun 13;7(1):3424.  [Content Brief]

  [4]. Gallic acid induces necroptosis via TNF-α signaling pathway in activated hepatic stellate cells. Chang YJ, et al. PLoS One. 2015 Mar 27;10(3):e0120713.  [Content Brief]