sor-c13

SOR-C13 is an inhibitor of transient receptor potential cation channel vanilloid family member 6 (TRPV6, CaT1 or CATL) with potential antineoplastic activity. TRPV6 calcium channel inhibitor SOR-C13 binds to TRPV6 and prevents the influx of calcium ions into TRPV6-expressing tumor cells. This inhibits the activation of nuclear factor of activated T-cell (NFAT) transcription complex which may result in an inhibition of calcium-dependent cancer cell proliferation and an induction of apoptosis in tumor cells overexpressing TRPV6.

SOR-C13 TFA, a truncated carboxy-terminal peptide, serves as a potent TRPV6 antagonist, demonstrating high affinity with an IC 50 value of 14 nM. TRPV6, a non-voltage-gated calcium channel linked to malignancy and poor prognosis in breast cancer, is effectively targeted by SOR-C13 TFA, indicating its anticancer activity [1].

Nifuroxazide-d4 is intended for use as an internal standard for the quantification of nifuroxazide by GC- or LC-MS. Nifuroxazide is a nitrofuran antibiotic. It is active against strains of the enteropathogenic bacteria C. jejuni, Salmonella, Y. enterocolitica, Shigella, and E. coli. It inhibits quorum sensing and virulence factor production in P. aeruginosa. Nifuroxazide inhibits STAT3 activity in a reporter assay and decreases viability of U266 and INA-6 myeloma cells, which have constitutive STAT3 phosphorylation, with EC50 values of approximately 4.5 µM for both. It also decreases viability, migration, and invasion of, and induces apoptosis in, MCF-7, 4T1, and MDA-MB-231 breast cancer cells. Nifuroxazide reduces tumor growth and prevents pulmonary metastasis in a 4T1 murine mammary carcinoma model. It also reduces diarrhea, weight loss, and colon inflammation in a rat model of acetic acid-induced ulcerative colitis.