Niraparib-treated mice with increased platelet production retain normal platelet function. Blood was drawn from vehicle- and niraparib-treated (25 mg/kg) mice and (A) Flow cytometry was used to measure mean fluorescence intensity (MFI) of αIIb integrins (CD41), GPIbα, and GPVI in resting platelets (n = 5 mice per group). Data are mean ± SD; unpaired, 2-tailed Student t test. (B-C) Platelets were activated with indicated agonists and surface P-selectin (B) and activated αIIbβ3 integrins (C) were measured by flow cytometry. n = 5 mice per group. Data are mean ± SD; multiple t tests were used. (D) Platelet aggregation was measured using washed platelets isolated from vehicle- and niraparib-treated mice that were treated with thrombin (0.5 U/mL), collagen (CRP, 1 μg/mL), ADP (10 μM), or thromboxane (1 μM). Absorbance at 450 nm was used to calculate total aggregation for each sample normalized to the positive and negative controls (n = 5 mice per group). Data are mean ± SD; unpaired 2-tailed Student t test. (E) Schematic of niraparib treatment and in vivo platelet depletion using an anti-GPIbα antibody (2 μg/g per mouse). (F) Platelet counts were measured after anti-GPIbα administration were measured over 6 consecutive days (n = 5 mice per group). Data are mean ± SD; unpaired, 2-tailed Student t test. CRP, collagen related peptide; Plt, platelet.