Bisphenol A (BPA), a typical environmental endocrine disruptor, induces transgenerational reproductive injury in animals and humans. This study aimed to investigate the effects and underlying mechanisms of Semen Cuscutae flavonoids (SCFs) against prenatal BPA exposure induced reproductive toxicity in male and female offspring mice. Pregnant Kunming mice were intragastrically administered corn oil (control), 50 mg/kg bw/d BPA (BPA group), or a combination of 50 mg/kg bw/d BPA and 1 mg/kg bw/d SCFs (SCFs group) from gestation day (GD) 1 to GD14. Serum, testes and ovaries from 8 weeks-old offspring mice were collected, and multiple reproductive-related indicators were detected via ELISA, TUNEL, immunohistochemistry (IHC) and RT-qPCR. Quantitative results showed that prenatal BPA exposure significantly reduced serum testosterone (T) in male offspring, elevated estradiol (E2) while suppressed follicle stimulating hormone (FSH) and luteinizing hormone (LH) in female offspring, accompanied by abnormal gonadal histomorphology and sharply increased gonadal apoptotic cells. At the molecular level, BPA downregulated steroidogenic genes StAR, CYP11α and folliculogenesis-related Kitlg, upregulated ovarian AMH, disturbed the balance of pro-apoptotic Bax and anti-apoptotic Bcl-2, and ultimately triggered gonadal cell apoptosis. SCFs intervention reversed BPA-induced hormonal disorders and gonadal histological lesions. Mechanistically, SCFs upregulated Bcl-2 and downregulated Bax genes to reduce gonadal apoptosis. Meanwhile, SCFs restored the mRNA and protein expression of StAR, CYP11α, Kitlg and AMH, which are critical regulatory factors for reproductive hormone secretion and follicular development. In conclusion, SCFs exert protective effects against prenatal BPA-triggered offspring reproductive toxicity by balancing apoptotic signaling and modulating steroidogenic and folliculogenic gene expression.