NVP-BHS345

NVP-BHS345 (0.1-200 μM; 30 h) inhibits growth of wild-type Saccharomyces cerevisiae by targeting TORC1 and TORC2, with co-expression of TOR1^M2282T and TOR2^M2286T conferring complete resistance to concentrations up to 200 μM^[1].
NVP-BHS345 (10 μM; 12 min) acutely inhibits both TORC1 and TORC2 activity in wild-type Saccharomyces cerevisiae, with TOR1^M2282T conferring partial TORC1 resistance and TOR2^M2286T conferring robust TORC2 resistance^[1].
NVP-BHS345 (15 μM; 90 min) acutely arrests fluid-phase endocytosis in Saccharomyces cerevisiae TOR1^M2282T cells via a Ypk1-dependent mechanism^[1].
NVP-BHS345 (15 μM; 30 min pre-incubation, followed by 30 min MM4-64 incubation with drug present) blocks lipid endocytosis in Saccharomyces cerevisiae TOR1^M2282T cells via a Ypk1-dependent mechanism, preventing vacuolar membrane accumulation of MM4-64^[1].
NVP-BHS345 (15 μM; 30-90 min) induces rapid, time-dependent actin depolarization in Saccharomyces cerevisiae TOR1^M2282T cells via a Ypk1-dependent mechanism, with half-maximal effect observed by 30 min^[1].
NVP-BHS345 (15 μM; 30-180 min) acutely inhibits TORC2 and activates the CWI pathway in Saccharomyces cerevisiae TOR1^M2282T cells, indicating actin depolarization induced by NVP-BHS345 is not caused by CWI pathway inactivation^[1].
NVP-BHS345 (15 μM; 30-90 min (actin polarization); 90 min (Lucifer Yellow uptake); 30 min pre-incubation followed by 30 min MM4-64 incubation with drug present (lipid endocytosis)) induced actin depolarization and endocytosis arrest that was largely suppressed by deletion of FPK1/2 in Saccharomyces cerevisiae TOR1^M2282T cells, identifying Fpk1/2 as major mediators of TORC2-dependent regulation of these processes^[1].
NVP-BHS345 (15 μM; 30 min) induces Ypk1-dependent, Fpk1/2-independent dephosphorylation of endocytic proteins Ent1 and Pan1 in Saccharomyces cerevisiae TOR1^M2282T cells, identifying a direct TORC2 signaling pathway to the endocytic machinery^[1].
NVP-BHS345 (100 μM; 15-60 min) inhibits both TORC1 and TORC2 in wild-type Saccharomyces cerevisiae cells, leading to complete dephosphorylation of Rps6 on Ser-232 and Ser-233 within 60 minutes of treatment with 100 μM^[2].
NVP-BHS345 (100 μM; 30-60 min)-induced Rps6 dephosphorylation is blocked in glc7-127 Saccharomyces cerevisiae cells, indicating the PP1 phosphatase Glc7 is required for this dephosphorylation event^[2].
NVP-BHS345 (100 μM; 30-60 min)-induced Rps6 dephosphorylation is blocked in shp1Δ Saccharomyces cerevisiae cells, indicating the Glc7 regulatory subunit Shp1 is required for this dephosphorylation event^[2].
NVP-BHS345 (10 μM; 70 min) enhances Zeocin-induced yeast chromosome shattering in wild-type Saccharomyces cerevisiae cells with Pan1 depletion, resulting in a B/A signal intensity ratio of 17^[3].
NVP-BHS345 (5-10 μM; 70 min) induces massive chromosome fragmentation in exponentially growing wild-type Saccharomyces cerevisiae when combined with Zeocin (25-75 μg/mL; 70 min), with full fragmentation occurring at 10 μM NVP-BHS345 and 75 μg/mL Zeocin, and this effect is partially dependent on functional base excision repair glycosylases^[4].
NVP-BHS345 potently inhibits the kinase activity of purified budding yeast Saccharomyces cerevisiae TORC1 and TORC2 complexes with an IC₅₀ of 1 μM^[5].
NVP-BHS345 (0.01-100 μM) does not significantly inhibit the kinase activity of immunoprecipitated budding yeast Mec1-Ddc2 complexes at concentrations up to 10 μM, with only partial inhibition observed at 100 μM^[5].
NVP-BHS345 (5 μM; 3 days) weakly enhances sgs1^Δ budding yeast sensitivity to HU and Camptothecin (HY-16560), while profoundly and uniformly sensitizing W303 wild-type, sgs1^Δ, and mec1-100 budding yeast strains to Zeocin and IR, reducing colony formation by ~1000-fold^[5].
NVP-BHS345 (10 μM; 2 hr) causes persistent hyperphosphorylation of the DNA damage checkpoint kinase Rad53 in Zeocin-treated budding yeast wild-type (GA-1981) cells, indicating unimpaired checkpoint activation^[5].
NVP-BHS345 (10 μM; 1 hr/ continuous exposure) drastically increases the percentage of budding yeast wild-type (GA-1981) cells with Rad52 foci (a marker of DSB repair) when combined with Zeocin or IR, indicating elevated or persistent DNA double-strand breaks^[5].
NVP-BHS345 (1-100 μM; 0-60 min) causes dose-dependent inhibition of TORC1 (measured via Sch9 phosphorylation) and complex dose-dependent effects on TORC2 activity (measured via Ypk1 phosphorylation) in budding yeast MS113 cells, with rapid inhibition of Ypk1 phosphorylation at 100 μM^[5].
NVP-BHS345 (50 μM; 2 days) inhibits growth of budding yeast wild-type cells, with partial resistance conferred by TORC1 or TORC2 bypass mutations and full resistance conferred by combined TORC1&TORC2 bypass mutations, indicating it targets both TORC1 and TORC2^[5].

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