MTP3

MTP3 (0.5-20 μM; 0.5-4 h) induces dose- and time-dependent loss of full-length MYC and formation of N-terminally truncated tMYC in PC3 prostate cancer cells, with no effect on MYC mRNA levels, and reduces the half-life of full-length MYC from 30.4 min to 15.7 min^[1].
MTP3 (20 μM; 2 h) induces tMYC formation in PC3, VCaP, DU145, and MCF7 cancer cell lines, but not in SUM159 or MV4-11 cell lines^[1].
MTP3 (10 μM; 2 h) induces CRBN-dependent tMYC formation in PC3 prostate cancer cells^[1].
MTP3-induced loss of full-length MYC in PC3 prostate cancer cells is partially proteasome-dependent, while tMYC formation is largely proteasome-independent, as Bortezomib (HY-10227) rescues 50% of full-length MYC levels but not tMYC levels^[1].
MTP3 (10 μM; 2 h) induces tMYC that localizes to the nucleus, like full-length MYC, in PC3 prostate cancer cells^[1].
MTP3 (20 μM; 96 h) does not reduce viability of PC3 prostate cancer cells, as MYC maintains oncogenic proliferative function^[1].
MTP3 (10 μM; 2 h treatment, 24 h post-wash) induces reversible MYC depletion in prostate cancer PC3 cells, with MYC levels recovering within 24 hours after a 2-hour 10 μM treatment and washout^[1].
MTP3 (20 μM; 24 h) does not alter MYC gene mRNA transcript read coverage in treated cells after a 24-hour 20 μM treatment^[1].
MTP3 (10-20 μM; 2 h) induces context-dependent MYC alteration, causing MYC truncation in breast cancer MCF7 cells and full-length MYC reduction in prostate cancer DU145 and VCaP cells, with no effect on GSPT1 levels, after a 2-hour treatment at 20 μM (MCF7) or 10 μM (DU145, VCaP)^[1].
MTP3 (10 μM; 2 h) induces N-terminal truncation of MYC in prostate cancer PC3 cells, with truncated MYC present in both cytoplasmic and nuclear fractions, after a 2-hour 10 μM treatment^[1].
MTP3 (20 μM; 24 h) induces subtle gene regulatory changes in PC3 prostate cancer cells, with tMYC serving as a functional proxy for full-length MYC in most gene regulatory processes^[1].
MTP3 (10-40 μM; 72 h) enhances the anti-proliferative efficacy of nonsteroidal antiandrogen agent, second-generation nonsteroidal antiandrogen agent, and taxane chemotherapy agent in both androgen receptor-independent PC3 cells and androgen receptor-dependent VCaP cells after 72 hours of combined treatment at concentrations of 10-40 μM^[1].

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