TPP2a bromide

TPP2a (5 min at 25 °C) potently inhibits purified mammalian TrxR with an IC₅₀ of 1.16 μM^[1].
TPP2a (24 h) potently inhibits mitochondrial TrxR isolated from HeLa cells with an IC₅₀ of 1.44 μM, a 16.8-fold improvement over its parental compound 2a^[1].
TPP2a selectively and covalently binds to the Sec498 residue of TrxR, as demonstrated by fluorescent labeling of TrxR in HeLa cell lysates and purified TrxR samples, and dose-dependent inhibition of BIAM labeling at pH 6.5^[1].
TPP2a (1.0 μM; 6 h) selectively localizes to the mitochondria of living HeLa cells, as shown by colocalization with MitoTracker Red in confocal microscopy images^[1].
TPP2a, when coupled with a Cu²⁺-based nonspecific signal quenching strategy, acts as a selective fluorescent probe for TrxR, exhibiting specific fluorescence in purified TrxR samples, TrxR-depleted HeLa cell lysates, and living HeLa cells with intact mitochondrial TrxR^[1].
TPP2a (48 h) potently inhibits the growth of HeLa, PC3, A549, Bel-7402, MDA-MB-231, and SW480 human cancer cell lines with IC₅₀ values ranging from 0.91 μM to 2.77 μM, with HeLa cells being the most sensitive^[1].
TPP2a (0.1-2.5 μM; 6 h) dose-dependently increases superoxide anion and hydrogen peroxide levels in HeLa cells after 6 h of incubation, with maximal effects observed at 2.5 μM^[1].
TPP2a (0.1-2.5 μM; 24-48 h) dose-dependently induces apoptosis in HeLa cells via the intrinsic mitochondrial pathway, with 96.80% total apoptotic cells observed at 2.5 μM, accompanied by decreased mitochondrial membrane potential, altered Bcl-2 family protein expression, and activation of caspase and PARP cleavage^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.