Niagen Bioscience (NASDAQ: NAGE) highlighted independent preclinical research published in Nature Communications identifying the CD38 enzyme as a primary driver of age-related NAD+ decline in placental tissue.

The study, led by researchers at Sichuan Agricultural University, analyzed human, mouse, and pig models. It found that older mothers exhibited lower levels of NAD+, NADH, and NADP+ in placental tissue compared to younger mothers. Higher metabolite levels correlated with higher infant birth weights across species.

Andrew Shao, PhD, Senior Vice President of Global Scientific and Regulatory Affairs at Niagen Bioscience, stated the paper demonstrated age-related decline in placental tissue NAD+, reaffirmed that CD38 consumes both NAD+ and NMN, and showed the positive reproductive effects of increasing NAD+ with NR.

Mechanism and Precursor Dynamics

The research identified CD38-expressing macrophages accumulating in aged placental tissue as the source of depletion. These cells consumed NAD+ from neighboring decidual stromal cells. The authors noted that CD38 acts extracellularly, degrading precursors before they can enter cells. CD38 is a multifunctional ectoenzyme whose expression increases with age, particularly on immune cell surfaces, contributing to metabolic changes and inflammation.

The study distinguished between two NAD+ precursors:

• Nicotinamide mononucleotide (NMN): CD38 degrades NMN outside the cell. Because NMN carries a phosphate group, it cannot cross the cell membrane intact and remains exposed to degradation.
• Nicotinamide riboside (NR): Previous research cited by the authors indicates NR inhibits CD38 activity. Consequently, NR is not consumed by CD38 outside the cell.

Experimental Outcomes

In aged pregnant mice, oral NR administration or CD38 inhibition restored placental NAD+ levels. This intervention improved fetal growth and shifted placental gene expression toward a younger profile. The company clarified it did not conduct, fund, or design the study, nor was its proprietary Niagen ingredient used.

What the Numbers Show

The data reveals a divergence in precursor efficacy based on enzymatic activity. While both NMN and NR aim to boost NAD+, the presence of high CD38 activity creates a barrier for NMN due to extracellular degradation. NR’s dual role as a precursor and CD38 inhibitor suggests a structural advantage in tissues where this enzyme is overactive, such as aged or inflamed placental tissue.

Broader Research Context

The findings align with a broader body of preclinical evidence regarding NR and reproductive endpoints. Previous studies listed by the company include:

• Improved mitochondrial function in PCOS patients (Wang et al., 2021).
• Enhanced lactation and offspring development in sow models (Huang et al., 2025/2026).
• Reversal of ovarian aging and improved oocyte quality in mice (Yang et al., 2020/2023; Li et al., 2022).
• Protection against gestational hypoxia effects in fetal guinea pigs (Thompson et al., 2023).

Niagen Bioscience, Inc. (NASDAQ: NAGE) will participate in the Longevity Investors Conference in Gstaad, Switzerland, from September 14 to 17, 2026. Senior management aims to engage with institutional investors and scientists on the company’s NAD+ science strategy.

CEO Rob Fried will speak on the "Longevity Goes Mainstream: The Investment Case for Consumer Health" panel on Wednesday, September 16, from 14:50 to 15:30 p.m. CEST. He will be joined by Chief Financial Officer Ozan Pamir for one-on-one investor meetings throughout the event.

Conference Details

The conference features discussions on breakthrough research shaping the longevity sector. Attendees can sample Tru Niagen and experience Niagen Plus on-site. The event targets institutional investors, family offices, and funds.

Investors seeking meetings should contact their conference representative or email Niagen@KCSA.com . Niagen Bioscience remains the global authority on NAD+ science, focusing on healthy aging through its patented nicotinamide riboside technology.