ipm

Palifosfamide (Isophosphamide mustard) lysine (ZIO-201) is a stable form of palifosfamide. Palifosfamide lysine has broad activity in sarcoma lines in vitro. The IC50 ranges from 2.25 to 6.75 μM for most cell lines except OS222 (IC50=31.5 μM).

Isopropyl myristate (IPM) is an ester formed from isopropyl alcohol and myristic acid.

BIPM is a potent inhibitor of Rho-associated protein kinase 2 (ROCK2). Exposure of SH-SY5Y cells to BIPM led to significant changes in cell migration, actin stress fibers and neurite length. BIPM significantly inhibits phosphorylation of cofilin, a regula

FAM-DEALAHypYIPMDDDFQLRSF is a 5,6-carboxyfluorescein (FAM) labeled HIF-1α peptide. It binds with high affinity to von Hippel-Lindau (VHL) protein (KD= 3 nM). Can be used to assess ligand binding to VHL in a direct fluorescence polarization (FP) displacement assay. Excitation/emission maxima (λ) = 485/520 nm. This product is a longer peptide version of FAM-DEALA-Hyp-YIPD.

Evofosfamide (TH-302) is a hypoxia-activated prodrug of the cytotoxin bromo-isophosphoramide mustard (Br-IPM) conjugated with 2-nitroimidazole, possessing potential antineoplastic activity. Under hypoxic conditions, typical of hypoxic tumors, the 2-nitroimidazole moiety is reduced, releasing the DNA-alkylating Br-IPM moiety, which induces intra- and inter-strand DNA crosslinks that inhibit DNA replication and cell division, potentially causing apoptosis in tumor cells. The inactive form of the prodrug remains stable under normoxic conditions, which may reduce systemic toxicity.

Palifosfamide (tromethamine), a synthetically derived alkylating agent, exhibits potential antineoplastic properties. Acting as the stabilized active metabolite of ifosfamide, it irreversibly alkylates and crosslinks DNA at GC base pairs, inhibiting DNA replication and inducing cell death. Palifosfamide (tromethamine) boasts reduced toxicity in comparison to ifosfamide.

2-Isopropylmalic acid (α-Isopropylmalate) inhibits excess reactive oxygen species (ROS) production and stress kinase activation in PM2. 5-treated dermal fibroblasts, promotes primary ciliogenesis and restores PM2. 5-induced primary ciliogenesis hypoplasia in dermal fibroblasts.