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. 2024 May 11;14(7):2993–3013. doi: 10.7150/thno.97320

Table 2.

Small-molecule compounds targeting SIRT5 for cancer therapy

Name Chemical structure mechanism Cancer cell type IC50 Pharmacological interventions Preclinical tumor model Ref.
MC3482 graphic file with name thnov14p2993i021.jpg MC3428-mediated SIRT5 inhibition led to an increase in intracellular ammonia and promoted ammonia-induced autophagy and mitosis MDA-MB-231 42% inhibition of SIRT5 at 50 μM 50μM MC3482 is treated in MDA-MB-231 for 24 h. No in vivo experiment information is available. / 95
MC3183 graphic file with name thnov14p2993i022.jpg SIRT5-GOT1-glutamine metabolism pathway CFPAC, FG, PANC1, S2-013, Canpan1, S2-007, T3M4, Patu8902, MIAPaCa-2, Capan2 IC50 = 25.4 - 236.9 μM PDAC cells are treated with 10μM MC3183 for 24 h. The maximum concentration and half-life of MC3138 in plasma are approximately 230 μM and 5.059 hours, respectively. In the PDX tumor model of NOD-SCID mice, when the concentration of MC3183 in tumor tissue is around 100~200μM, the combined use of MC3183 and gemcitabine can effectively inhibit PDAC growth. PDX models of pancreatic cancer 92
NRD167 graphic file with name thnov14p2993i023.jpg NRD167 induced apoptosis through oxidative stress and the glutamine metabolism pathway SKM-1 and OCI-AML2 IC50 = 5-8 μM 5-10μM in AML cells and no in vivo experiment information is available. Xenograft mouse models using CMK and OCI-AML3 cells 119