Inz-1 

Inz-1 is a potent and selective mitochondrial cytochrome bc1 inhibitor for yeast (IC₅₀=8.092 μM) over humans (IC₅₀=45.320 μM). Inz-1 reverses Fluconazole (HY-B0101) or other triazole antifungals’ resistance in the pathogenic fungus Candida albicans^[1].

IC50: 8.092 μM (yeast mitochondrial cytochrome bc1)
IC50: 45.320 μM (human mitochondrial cytochrome bc1)^[1]

Inz-1 (0-16 μM; 24 hours) inhibits the growth of the model yeast S. cerevisiae (strain BY4741) and C. albicans (SC5314) in media containing glucose or glycerol as the sole carbon source, while only mildly slowing growth in glucose^[1]. 
Inz-1 (0-100 μM; 24 hours) shows inhibition of yeast cytochrome B enzymatic activity in a concentration -dependent manner in both wild-type and F90Y mutant mitochondria. It exhibits inhibition of cytochrome bc1 from both S. cerevisiae and C. albicans with IC₅₀ value of 2.5 μM and 8.0 μM, respectively^[1].
Inz-1 (0-100 μM; 24 hours) is selective for yeast over human cytochrome bc1, it inhibits human cytochrome bc1 activity only weakly, with an IC₅₀ of 45.3 μM, 5.6-fold higher than the IC₅₀ for the C. albicans homolog in mitochondria purified from HEK293 human embryonic kidney cells^[1].
Inz-1 (0-100 μM; 24 hours) inhibits proliferation under forced respiration conditions only at 32 μM，and only mildly at that concentration^[1].
Inz-1 is against candida, human enzyme with IC₅₀ values of 8.092 μM and 45.320 μM, respectively. It against Candida and HepG2 respiring growth with IC₅₀ values of 1.655 uM and >32 μM, respectively^[1].

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

266.29

C₁₆H₁₄N₂O₂

897776-15-7

O=C(OC)CN1N=C(C2=CC=CC=C2)C3=C1C=CC=C3

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Benjamin M Vincent, et al. A Fungal-Selective Cytochrome Bc 1 Inhibitor Impairs Virulence and Prevents the Evolution of Drug Resistance.Cell Chem Biol. 2016 Aug 18;23(8):978-991.  [Content Brief]