Pyridostatin trihydrochloride

Pyridostatin (2 μM; 72 h) trihydrochloride potently inhibits the proliferation of SV40-transformed human MRC5 fibroblasts^[1].
Pyridostatin (2 μM; 1-10 days) trihydrochloride induces G2-phase cell cycle arrest and activates the DNA damage response in SV40-transformed human MRC5 fibroblasts and various human cancer cell lines. Long-term treatment causes G1-phase arrest in some cells, and checkpoint inhibition reverses this cell cycle arrest^[1].
Pyridostatin (2 μM) trihydrochloride induces DNA double-strand breaks (DSBs) in SV40-transformed human MRC5 fibroblasts. DNA-PKcs mediates sustained DSB repair during treatment, and DNA-PKcs-deficient MO59J cells are more sensitive to Pyridostatin than MO59K cells with normal DNA-PKcs expression^[1].
Pyridostatin (2 μM) trihydrochloride induces transcription-dependent DNA damage in SV40-transformed human MRC5 fibroblasts at the G1 and G2 phases, while it induces both transcription-dependent and replication-dependent DNA damage in S-phase cells^[1].
At low concentrations, Pyridostatin (2 μM; 24 h) trihydrochloride primarily targets non-telomeric DNA sites in SV40-transformed human MRC5 fibroblasts, whereas telomeric targeting occurs at higher doses, and inhibition of DNA-PKcs enhances Pyridostatin-induced mitotic chromosomal DNA damage^[1].
Pyridostatin (2 μM; 8-24 h) trihydrochloride induces DNA damage (γH2AX enrichment) in gene ontologies containing clusters of G-quadruplex-forming sequences, including the human proto-oncogene SRC, and downregulates the mRNA levels of these damaged genes in SV40-transformed human MRC5 fibroblasts^[1].
Pyridostatin (2 μM; 24 h) trihydrochloride reduces SRC protein levels by approximately 60% in SV40-transformed human MRC5 fibroblasts^[1].
Pyridostatin (2 μM; 24 h, 48 h) trihydrochloride reduces SRC-dependent cell motility in MDA-MB-231 human breast cancer cells, and its mechanism of action may involve downregulating SRC mRNA and protein levels rather than inducing widespread DNA damage^[1].
Pyridostatin (10 μM; 24 h) trihydrochloride alters the proteome of human HeLa cervical cancer cells, significantly downregulating 22 proteins including SUB1 (4.76-fold) while upregulating 16 proteins, and most of the affected genes contain potential G-quadruplex sequences^[2].
Pyridostatin (10 μM; 24 h) trihydrochloride regulates gene transcription in human HeLa cervical cancer cells in a sequence-dependent manner, significantly downregulating THRAP3, ARL6IP4 and GPC1, but exerts no such effect on SUB1 or COL5A1^[2].
Pyridostatin (2-10 μM; 24 h) trihydrochloride downregulates the expression of PC4 protein in human HeLa cervical cancer cells in a concentration-dependent manner, and treatment with 10 μM for 24 h almost completely abolishes the expression level of PC4^[2].
Pyridostatin (10 μM; 24 h) trihydrochloride increases the accumulation of trans-PtTz in human HeLa cervical cancer cells, as detected by ToF-SIMS imaging^[2].
Pyridostatin (10 μM; 24 h) trihydrochloride increases the platinum modification level of genomic DNA in human HeLa cervical cancer cells by 4-fold compared with treatment with trans-PtTz alone^[2].
Pyridostatin (2 μM; overnight) trihydrochloride alters the transcriptional processes of primary mouse cortical neurons cultured in vitro for 14 days, differentially regulates 901 genes, and enriches pathways including nervous system development, immune response and p53 signaling pathway, among which the Pirh2 gene is significantly up-regulated^[3].
Pyridostatin (2 μM; overnight) trihydrochloride induces distinct transcriptional responses in primary cortical neurons cultured in vitro for 4 days and 14 days, significantly downregulating Atg7 and Brca1 in immature neurons, while upregulating Pirh2 in both immature and mature neurons^[3].
Pyridostatin (2 μM; overnight) trihydrochloride modulates the morphology of BFP-Pirh2-positive intranuclear foci in primary cortical neurons, enhancing the intensity and reducing the area of the foci^[3].
Pyridostatin (2 μM; overnight) trihydrochloride enhances the colocalization of nucleolar DDX21 and nucleolin in primary cortical neurons, which is associated with nucleolar condensation^[3].
Pyridostatin (1.25-20 μM) trihydrochloride binds with high affinity to G-quadruplexes in 3'-UTR, NS3, NS5A and NS5B RNAs of Zika virus (ZIKV), with the highest affinity for NS5A (K_A = 36.7 μM)^[4].
Pyridostatin (400 μM) trihydrochloride forms stable complexes with the 3'-UTR, NS3, NS5A and NS5B G-quadruplexes of Zika virus (ZIKV) RNA, among which the binding affinity with NS5A is the highest (K_A = 40.0 μM)^[4].
Pyridostatin (10 μM; 2 h) trihydrochloride binds to and stabilizes the ZIKV NS5A RNA G-quadruplex in the cytoplasm of Vero cells, increasing the detectable level of stable RNA G-quadruplex structures^[4].
Pyridostatin (10 μM; 4 days) trihydrochloride potently reduces the cytopathic effect induced by Zika virus (ZIKV) in Vero cells^[4].
Pyridostatin (0.625-25 μM; 3-4 days) trihydrochloride exhibits potent anti-Zika virus (ZIKV) activity in Vero cells, with an EC₅₀ of 4.2 μM, and shows low cytotoxicity, maintaining >85% cell viability even at concentrations as high as 25 μM^[4].
Pyridostatin (1.25-10 μM; 72 h) trihydrochloride inhibits ZIKV mRNA replication and the mRNA expression of E and NS1 proteins in Vero cells in a dose-dependent manner, and reduces viral mRNA levels by > 94% at a concentration of 10 μM^[4].
Pyridostatin (2.5-10 μM; 72 h) trihydrochloride inhibits the expression of ZIKV E and NS1 proteins in Vero cells in a dose-dependent manner, with a significant reduction in expression levels observed at concentrations of 5 μM and higher^[4].
Treatment with Pyridostatin (10 μM; 72 h) trihydrochloride reduces NS1 protein levels and the number of ZIKV-positive Vero cells^[4].

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