Preclinical reproductive study

Nicotinamide mononucleotide protects ovarian function and oocyte developmental competence during chemotherapy

Lin Shen et al. · Journal of Ovarian Research · 2025

Evidence type: Preclinical mechanistic study Interpretive weight: Mechanistic contextResearch area: Ovarian function during chemotherapy
DesignControlled 14-day mouse chemotherapy model with ovarian, oocyte, embryo-development, oxidative-stress, DNA-damage, apoptosis, and transcriptomic analyses.
PopulationEight-week-old female C57 mice; no human participants.
SampleCore ovarian comparisons generally used approximately 6 mice per group, with separate oocyte and embryo samples and five replicate IVF experiments.
InterventionCyclophosphamide 150 mg/kg intraperitoneally on days 1 and 6; NMN 200 mg/kg intraperitoneally once nightly from day 0 through day 13 in the NMN+CTX group.
EndpointsOvarian NAD+ and NAD(H); Follicle counts, ovarian reserve, AMH, FSH, and ovary index; Oocyte yield, ROS, DNA damage, and apoptosis; Ovarian and oocyte transcriptomic changes; Two-cell embryo and blastocyst formation; Blastocyst cell count, ROS, DNA damage, and apoptosis

What the publication reported

This animal study tested whether NMN could reduce ovarian and oocyte damage during cyclophosphamide treatment.

Compared with cyclophosphamide alone, the NMN-plus-cyclophosphamide group had higher ovarian NAD+, better follicle and endocrine measures, lower oxidative-stress and DNA-damage signals, and less apoptosis. Oocyte yield and several embryo-development measures were also improved.

Transcriptomic analyses identified candidate pathways and genes that changed with cyclophosphamide and were partly restored with NMN. These results come from mice receiving intraperitoneal NMN and do not establish fertility preservation in human cancer patients.

Key findings

  • NMN supplementation increased ovarian NAD+ and NAD(H) during cyclophosphamide exposure.
  • Follicle counts and ovarian endocrine/reserve measures were improved relative to cyclophosphamide alone.
  • Oocyte oxidative stress, DNA-damage signaling, and apoptosis measures were reduced with NMN.
  • Two-cell embryo and blastocyst formation rates improved in the NMN-plus-cyclophosphamide group.
  • Blastocyst cell number increased while oxidative-stress, DNA-damage, and apoptosis measures decreased.
  • Ovarian and oocyte transcriptomics identified candidate genes including Banp, Rbm47, and Sgk1 as potential mediators.

What it cannot establish

  • The study used a mouse cyclophosphamide model, not patients receiving cancer therapy.
  • NMN was administered intraperitoneally at 200 mg/kg, not as routine oral supplementation.
  • Core comparisons used small animal groups and multiple downstream oocyte/embryo subsamples.
  • Improved embryo-development measures in vitro do not establish live-birth outcomes or long-term offspring safety.
  • The study did not establish whether NMN alters cyclophosphamide's antitumor effectiveness.
HealthspanX claim boundary: This study does not establish that NMN preserves fertility in people receiving chemotherapy, is safe to combine with cancer treatment, or improves human pregnancy or live-birth outcomes.

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