Canventol

Canventol (0.1-100 μM; 1 h pre-incubation, 24 h incubation with Okadaic acid (HY-N6785)) dose-dependently inhibits Okadaic acid (HY-N6785)-induced mTNF-α release from BALB/3T3 cells, with an IC₅₀ of 21.0 μM^[1].
Canventol (500 μM-1 mM; 4 h) significantly inhibits protein prenylation in NIH3T3 cells, exerting prominent effects on proteins with a relative molecular mass (M_r) of 22000, 17000, and 13000, without reducing cell viability^[1].
Canventol (0.1-100 μM; pretreated for 1 h followed by co-treatment with 0.2 μM Okadaic acid for an additional 8 h) inhibits okadaic acid-induced TNF-α mRNA expression in BALB/3T3 cells at concentrations greater than 10 μM, suggesting that it suppresses TNF-α production at the transcriptional level^[2].
Canventol (100-500 μM; 18 h) regulates mevalonate metabolism in NIH/3T3 cells, increasing the ratio of sterols to ubiquinones (IPI index) to 8.2 at 500 μM for 18 h, which correlates with the indirect inhibition of protein isoprenylation^[1].
Canventol (1 mM; 4 h) inhibits protein prenylation in NIH/3T3 cells, reducing the radioactivity of 28-26 kDa geranylgeranylated proteins to 39.2% of the control level and that of 53 kDa farnesylated proteins to 41.8% of the control level^[1].
Canventol does not directly inhibit FPTase or GGPTase-I in vitro, indicating that its inhibition of protein isoprenylation is more likely derived from the regulation of intracellular mevalonate metabolism rather than direct blockade of protein isoprenyltransferases^[3].

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