Pinafide

Pinafide is an orally active anticancer agent. Pinafide binds to double-stranded DNA via intercalation, stabilizes the DNA-topoisomerase II complex, induces photo-induced DNA damage and ROS production, causes lysosomal and mitochondrial dysfunction, impairs DNA and RNA synthesis, and blocks cell growth. Pinafide binds to human serum albumin in vitro, undergoes biotransformation via reduction and acetylation in rats, and can cross the placental barrier of pregnant rats. Pinafide can be used in cancer-related research such as hepatocellular carcinoma^[1][2]. In Vitro:Pinafide (10-50 μg/mL) binds to human serum albumin, with one high-affinity, low-binding-capacity site (K₁ = 2.8×10⁶ M^-1) and one moderate-affinity, high-binding-capacity site (K₂ = 5.3×10³ M^-1)^[1].
Pinafide is a classic DNA intercalator that stabilizes calf thymus DNA, with a ΔT_m of 6.50 °C and a binding constant of 6.60 × 10⁴ M^-1[2].
Pinafide potently inhibits the proliferation of human hepatocellular carcinoma HepG2 cells, with an IC₅₀ value of 1.23 μM; when applied at the IC₅₀ concentration of 1.23 μM, it induces G2/M phase cell cycle arrest in human hepatocellular carcinoma HepG2 cells^[2].
Pinafide (0.615 μM; 24 h) induces reactive oxygen species production in human hepatocellular carcinoma HepG2 cells^[2]. In Vivo:Pinafide (20 mg/kg; i.v.; single bolus; p.o.; single dose) exhibits biphasic plasma disposition after i.v. administration, nearly complete oral bioavailability, and undergoes biotransformation via reduction and acetylation in healthy female Sprague-Dawley rats^[1].
Pinafide (10 mg/kg; i.v.; single bolus) crosses the placental barrier in pregnant Sprague-Dawley rats, with fetus and amniotic fluid concentrations exceeding or matching maternal blood concentrations 1 hour after i.v. administration^[1].