DC-LC3in-D5 is a chemical compound that functions as an autophagy inhibitor by diminishing the process of LC3B lipidation. It forms a binding association with LC3B, disrupting the LC3B-LBP2 interaction with an IC50 of 200 nM. This compound, DC-LC3in-D5, exhibits potential for application in anti-HCV or combination cancer treatments by effectively inhibiting autophagy [1].

DC-LC3in-D5 demonstrates high selectivity to LC3A/B in the proteome. DC-LC3in-D5 exhibits a potent covalent reactivity and selectivity to LC3A/B in HeLa cells [1]. Treatment of HeLa cells with DC-LC3in-D5 (3-30 μM) results in disruption of LC3B lipidation, inhibition of autophagic vesicle formation, and accumulation of p62 [1]. Western Blot Analysis [1] Cell Line: HeLa cells Concentration: 3, 10, 30 μM Incubation Time: 16 hours Result: Pre-treated accumulated significant more p62 than DMSO-treated control samples. Attenuated LC3-I/II lipidation in cells exposed to autophagy inducing conditions.