Valrubicin (AD-32) (AD 32) inhibits TPA- and PDBu-induced PKC activation (IC50s: 0.85 and 1.25 μM) and has antitumor and anti-inflammatory activity.

PKC (TPA-activated):0.85 μM, PKC (PDBu-induced):1.25 μM

Valrubicin抑制了[3H]PDBu与PKC的结合。因此，Valrubicin与肿瘤促进剂竞争PKC结合位点，阻止后者与磷脂相互作用及与PKC结合[1]。Valrubicin对鳞状细胞癌(SCC)细胞系集落形成显示出细胞毒性活性，其IC50s和IC90s分别为UMSCC5细胞8.24 μM和14.81 μM，UMSCC5/CDDP细胞15.90 μM和29.84 μM，以及UMSCC10b细胞10.50 μM和19.00 μM [2]。

Valrubicin（3、6或9 mg）通过在仓鼠体内肿瘤注射，在第三周显著减缓肿瘤生长。配合最小细胞毒性辐射（150、250或350 cGy）的Valrubicin（6 mg）在仓鼠体内显著缩小肿瘤体积[2]。Valrubicin（0.1 μg/μL）在挑战TPA的活组织切片中，显著减少24小时内渗透的中性粒细胞数量，并缓解小鼠的慢性炎症。Valrubicin还减少急性模型中炎症细胞因子的表达水平[3]。

UMSCC5 cells exposed to Valrubicin (2 μM for 3 h), a single dose of radiation (400 cGy), or the combined treatment are cultured for a further 12, 24, or 48 hours. At these times, the cells are collected by trypsinization (0.25%), washed in PBS, and fixed at 5 × 10^6 cells/mL with 95% ethanol. Cells are incubated with ribonuclease (50 μg; 70-90 Kunitz units/mg for 30 min), and the resulting pellet resuspended in and incubated with propidium iodide (0.05 mg/mL for 10 min). The DNA content of the samples is determined by flow cytometry according to standard technique [2].

Hamsters with cheek pouch tumors of 100 mm2 are randomly assigned to one of five treatment groups. Momentarily anesthetized animals each receives once a week × 3 injections (27 g × 0.5-inch needle: 0.1 mL administered slowly to the base of the lesion) of Valrubicin (3, 6, or 9 mg) or drug vehicle (Cremophor: alcohol;1:1 by volume; NaCl diluent 12). A further group of animals receives anesthesia but no direct tumor treatment (control). Individual tumor sizes are measured with calipers at weekly intervals for 4 weeks, at which time the animals are sacrificed [2].