Distamycin A hydrochloride

Distamycin A (1.2 × 10^-6 M; 2-5 min) hydrochloride mainly inhibits RNA chain initiation by E. coli RNA polymerase on T4-DNA; when the Distamycin/DNA ratio is 1:10, [¹⁴C]UMP incorporation decreases to 2.5% of the control, whereas preincubation renders the system resistant^[1].
Distamycin A (6-20 μM) hydrochloride inhibits DNA-dependent DNA polymerase (from Ehrlich ascites tumor cells) at 6 μM by binding to the DNA template, and inhibits RNA polymerase (from Escherichia coli) with a 50% inhibitory concentration of 10-20 μM^[4].
Distamycin A (20 h) hydrochloride induces resistance in Bacillus subtilis strains PB 1689, PB 1717, and PB 1718, with a minimum inhibitory concentration of 200 μg/mL, compared to 20 μg/mL for the parental strain PB 202^[7].
Distamycin A (50 μg/mL) hydrochloride induces a dst-3 mutation in Bacillus subtilis PB 1689, conferring resistance to growth inhibition, with the mutant being affected only at doses above 100 μg/mL compared to 50 μg/mL for the parental strain PB 202^[7].

Distamycin A (48 h) hydrochloride exhibits low cytotoxic activity against L1210 mouse leukemia cells with an IC₅₀ of 10069 nM^[6].
Distamycin A (48 h) hydrochloride shows cross-resistance in both Doxorubicin (HY-15142A)- and Tallimustine (HY-105270)-resistant L1210 leukemia cell lines, with IC₅₀ values of 459 μM and 142 μM, respectively^[6].

Distamycin A (2-3 μg/mL) hydrochloride protects Bacillus subtilis cells from SPP1 phage-induced lysis, possibly through osmotic stabilization of the cell envelope, without affecting phage infection and proliferation^[7].

Distamycin A hydrochloride inhibits DNA-dependent DNA synthesis using natural herring sperm DNA as a template^[1].
Distamycin A hydrochloride shows similar effectiveness against SV40 DNA and calf thymus DNA in RNA polymerase assays^[1].
Distamycin A (20-80 µM; 15 min) hydrochloride selectively inhibits the binding of transcription factors SRF and MEF2 to their respective A/T-rich elements in nuclear extracts of C2C12 myotubes, without affecting the binding of Sp1 or MyoD^[2].
Distamycin A (20-40 µg/mL; 3 days) hydrochloride reversibly inhibits the morphological differentiation of C2 myoblasts without significantly affecting cell growth^[2].
Distamycin A (20-40 µg/mL; 7 days) hydrochloride enhances adipocyte differentiation by approximately 4-fold in pluripotent TA1 cells while inhibiting myogenic differentiation by 85%^[2].
Distamycin A (40 µg/mL) hydrochloride strongly downregulates endogenous muscle-specific gene transcripts (cardiac α-actin, skeletal α-actin, myosin heavy chain, and myoD1) in differentiating C2 cells without affecting non-muscle gene transcripts^[2].
Distamycin A (40 µg/mL; 48 h) hydrochloride inhibits human cardiac α-actin promoter activity by 73% and human skeletal muscle α-actin promoter activity by 35% in C2 cells, while it does not inhibit the β-actin or c-fos promoter^[2].
Distamycin A (20-80 µg/mL; 48 h) hydrochloride inhibits the human cardiac α-actin promoter in a dose-dependent manner in CV-1 cells, even upon ectopic expression of myoD, indicating that this inhibition is not due to suppression of myoD expression^[2].
Distamycin A (40 µg/mL; 48 h) hydrochloride selectively inhibits MEF2-dependent promoter activity by 82% in CV-1 cells, while it does not inhibit MyoD-dependent promoter activity^[2].