Article: NAD+ and Cancer: Current Research on Supplementation Safety and Risk

Feb 2, 2026 Cancer In The News

NAD+ and Cancer: Current Research on Supplementation Safety and Risk

Key Takeaways

Cancer is complex and multifactorial: While NAMPT and NAD+ may be altered in cancer cells, they are not the cause of cancer—genetic mutations that impair growth regulation are the true driver.
NAD+ is essential for all cells: Cancer cells need NAD+ just like healthy cells do. However, this does not mean increasing NAD+ through supplementation causes or exacerbates cancer.
Preclinical findings can be misleading: In vitro and rodent studies are frequently overstated or sensationalized in media reports. Human biology and real-world scenarios differ significantly from laboratory conditions.
Human evidence to date suggests NAD+ precursors appear to be safe: Decades of research on NR and other NAD+ precursors have not shown increased cancer risk or major safety concerns in humans, though research is ongoing. Some preclinical studies even suggest possible protective effects.
Balanced communication and ongoing research are essential: Understanding the relationship between NAD+ and cancer requires careful interpretation of evidence, continued investigation, and responsible messaging to prevent misinformation.

Interest in anti-aging and longevity has grown substantially in recent years, encompassing strategies ranging from dietary supplements to infusions and injections. Among these, NAD+ (nicotinamide adenine dinucleotide) has emerged as a key focus, given its essential role in cellular metabolism, energy production, DNA repair, and other processes that support healthy aging. Because NAD+ levels naturally decline with age, approaches aimed at maintaining or restoring NAD+ have become a major focus in aging research.

Alongside this growing interest, some reports have raised concerns about a potential link between NAD+ and cancer. Sensational headlines and viral articles often cite preliminary animal or in vitro studies, often taking them out of context, contributing to misinformation, confusion, and understandable concern. Given the complexity of cancer biology and NAD+’s fundamental role in cellular processes, it is essential to distinguish between well-supported scientific evidence and oversimplified or misleading claims.

This pattern is not unique to NAD+, as other nutrients or supplements have experienced similar cycles of hype, backlash, and eventual clarification through further, more rigorous research. One example is vitamin D, which experienced a rapid surge and widespread hype in the 2000s,¹ followed by a period of conflicting headlines and public skepticism, before a stronger evidence base emerged to establish its benefits and safety.² NAD+ appears to be following a similar trajectory of early excitement, some overstated fears, and, now, a growing body of research helping provide more insight into its benefits.

This article will examine the current state of research on NAD+ and cancer, assess the validity of common concerns with respect to what the science currently shows, and review what is known about the safety of NAD+ supplementation. Cancer is not a single disease, and its complexity means that there is no simple or definitive answer regarding the relationship between NAD+ levels and cancer risk. While research in this area continues to evolve, available human data do not suggest harm from NAD+ precursors—and nicotinamide riboside (NR) is among those with relatively well-characterized safety data to date.

What Is NAD+ and How Is It Linked to Cancer?

NAD+ (nicotinamide adenine dinucleotide) is a coenzyme found in all living cells and is essential for life. It plays a central role in cellular metabolism, DNA repair, and overall cellular resiliency.³ As a key regulator of energy production and cellular maintenance, NAD+ enables cells to efficiently convert nutrients into energy and respond to physiological stress—functions that are fundamental to healthy aging.

One of NAD+’s primary functions is in energy metabolism, specifically through glycolysis and oxidative phosphorylation.⁴ These pathways allow cells to convert glucose and other nutrients into adenosine triphosphate (ATP), the cell’s main energy currency. Efficient energy metabolism is essential for all tissues, particularly those with high energy demands such as the brain, skeletal muscle, and heart.

Beyond energy production, NAD+ is also critical for cellular repair and resilience. It serves as a required substrate for enzymes such as sirtuins⁵ and poly(ADP-ribose) polymerases (PARPs).⁶ Sirtuins regulate cellular stress responses, metabolic homeostasis, and genomic stability, while PARPs play a central role in detecting DNA damage and initiating repair processes. Together, these enzymes help maintain genomic integrity and support normal cellular function over the lifespan.

Because accumulated DNA damage and impaired repair mechanisms are well-established contributors to many diseases,⁷ including cancer,⁸ the role of NAD+ in supporting DNA repair and cellular resilience is generally considered supportive of cellular health rather than harmful. NAD+ metabolism is also linked to immune function,⁹ regulation of inflammation,¹⁰ and cellular stress signaling,¹¹ all of which are important for maintaining tissue health and reducing disease risk.

However, despite NAD+'s vital biological roles, questions have emerged in recent years about whether increasing NAD+ levels could inadvertently support cancer growth. These concerns largely stem from preclinical research, rather than human clinical evidence.

Several preclinical studies—most notably those involving genetically modified rodent models—have explored how altered NAD+ metabolism may affect cancer cell behavior. Under specific experimental conditions, some research suggests that elevated NAD+ availability could support the high metabolic demands of rapidly dividing cancer cells. A frequently cited example, discussed in more detail later in this article, is a study by Maric et al., 2022, which examined NAD+ metabolism in genetically engineered mouse models predisposed to cancer and reported that nicotinamide riboside (NR) availability influenced cancer metabolism in certain contexts.¹²

It is important to define what such findings represent. Preclinical research refers to early-stage studies conducted in laboratory settings using cell cultures or animal models—commonly rodents—to explore biological mechanisms and generate hypotheses. While these studies are essential for advancing scientific understanding and can sometimes inform human biology, their results cannot be directly extrapolated to human physiology in a 1:1 manner. Differences between animal models and humans, as well as other biological complexities, mean that findings may not always translate perfectly to clinical outcomes or real-world supplement use.

Crucially, these preclinical studies do not demonstrate that NAD+ supplementation causes cancer in humans, nor do they establish a causal link between increasing NAD+ levels and cancer initiation or progression in humans. Nevertheless, these preclinical findings have often been amplified in media coverage, contributing to public confusion and concern.

In the following sections, we will examine these issues in greater detail, including the limitations of the existing preclinical data and how current human safety evidence—particularly for nicotinamide riboside (NR)—fits into the broader scientific understanding of NAD+ supplementation.

The Complex Nature of Cancer: A Multifactorial Disease

Cancer is not a single disease with a single cause. It is a multifactorial process driven by the accumulation of genetic mutations over time, shaped by a combination of inherited susceptibility, environmental exposures, and lifestyle factors.¹³ These interacting variables determine whether a cell maintains normal growth control or progresses into malignancy.

At a basic level, cancer develops when mutations disrupt the normal pathways that regulate cell growth, division, and death. These mutations may arise from internal sources, such as DNA replication errors or inherited genetic variants, as well as external factors like chemical toxins, radiation, and infections. Lifestyle choices like alcohol use and smoking may also affect cancer risk by influencing mutation rates, immune function, hormonal signaling, and metabolism.¹⁴

A defining feature of cancer cells is their altered metabolism. Unlike most healthy cells, which generate energy primarily through oxidative phosphorylation when oxygen is available, many cancer cells rely heavily on glycolysis even in the presence of oxygen.¹⁵ This phenomenon, known as the Warburg Effect, reflects a metabolic shift that supports rapid cell division by providing both energy and the building blocks required for growth.¹⁶

Because glycolysis depends on a steady supply of NAD+, cancer cells often exhibit higher NAD+ demand to sustain their metabolism.¹⁷ However, this does not mean NAD+ itself causes cancer. Rather, it reflects how cancer cells hijack normal cellular functions to fuel uncontrolled growth.

Importantly, NAD+ is only one part of a complex biological system. Cancer cannot be explained by any single molecule, nutrient, or pathway. While NAD+ plays a role in cellular metabolism, cancer is shaped by many genetic, environmental, and cellular factors. Cancer cells change their metabolism after acquiring mutations, and the availability of NAD+ alone does not cause cancer.

Increasing NAD+ levels through supplementation has not been shown to cause cancer in humans. In fact, some preclinical studies suggest that raising NAD+ levels may have beneficial effects and, in certain contexts, may even help suppress tumor growth.¹⁸'¹⁹

These findings reinforce that cancer is complex and multifactorial: while NAD+ participates in metabolism that cancer cells use, it does not override the many factors that drive cancer risk. Because of its central role in energy metabolism, NAD+ and the enzymes controlling its production have become important areas of study in cancer biology.

Interest in NAD+ from Cancer Researchers

Given that cancer cells rely heavily on NAD+ to maintain energy production for their high metabolic needs, researchers have studied NAD+ and the enzymes that regulate its production as potential therapeutic targets.

One key enzyme involved in NAD+ biosynthesis is nicotinamide phosphoribosyltransferase (NAMPT). NAMPT catalyzes a rate-limiting step in the salvage pathway that regenerates NAD+ from nicotinamide. Some studies have observed elevated NAMPT levels in certain human cancer cells, including breast,²⁰ prostate,²¹ and ovarian²² cancers, as well as in colorectal tumors.²³ However, higher NAMPT expression does not automatically translate to increased NAD+ levels, nor does it indicate that NAD+ is causing cancer.

Cancer cells often increase NAMPT and other metabolic enzymes to meet high energy demands or cope with mitochondrial stress and redox imbalance. This means that higher NAMPT is usually a secondary adaptation—not a cause of cancer. These changes help cells survive and grow, but the root cause of cancer remains the accumulation of genetic mutations that disrupt normal growth control.²⁴ These mutations can affect multiple metabolic pathways, which explains why enzymes like NAMPT are altered.

Reducing the Supply of NAD+ May Harm All Living Cells—Not Just Cancer Cells

Given cancer cells’ reliance on NAD+, some researchers have explored NAMPT inhibitors as a way to reduce NAD+ levels and slow tumor growth.²⁵'²⁶ While this approach can affect cancer cells, it also carries significant systemic risks. As NAD+ is essential for the survival and function of all healthy cells, depletion can lead to serious side effects.

Human studies have shown dose-limiting toxicities with NAMPT inhibitors, including gastrointestinal, hematologic, and metabolic effects.²⁷ Animal studies also demonstrate harm to normal tissues when NAD+ production is reduced.²⁸ These findings highlight a key challenge: targeting NAD+ metabolism in cancer is difficult because lowering NAD+ can harm healthy cells as much as—or more than—cancer cells.

Addressing the Myth: Is Increasing NAD+ Linked to Cancer Risk? What the Science Shows

Supplementing with NAD+ precursors is a common and well-studied approach to boosting NAD+ levels. The most frequently used precursors are vitamin B3 forms—including niacin (nicotinic acid), nicotinamide (niacinamide), and nicotinamide riboside (NR)—as well as nicotinamide mononucleotide (NMN), which is not classified as a vitamin B3, but is an NAD+ precursor.

Importantly, more than a half-century’s worth of research involving high-dose NAD+ precursor supplementation²⁹—along with clinical studies of over 2,000 participants—has found no evidence linking these compounds to an increased risk of cancer in humans.³⁰

In fact, some studies suggest the opposite: supplementation with NAD+ precursors may be associated with a lower risk of certain cancers.³¹

For example, a large Australian randomized controlled trial found that nicotinamide supplementation significantly reduced the incidence of non-melanoma skin cancer.³¹ Additionally, data from the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2014 revealed an inverse association between niacin intake and mortality among cancer patients.³²

Clinical studies of NR also further support NAD+ precursor safety. In a study of adult survivors of childhood cancer, NR supplementation was not associated with any serious adverse events.³³ Additionally, while not conducted in a cancer-related population, long-term NR supplementation over two years in patients with ataxia telangiectasia reported no adverse effects.³⁴ While these findings are reassuring and include one of the longer-duration human studies to date, longer-term and broader population studies are still needed.

High-quality animal studies also suggest that NAD+ precursors may even have protective effects in certain cancer contexts. For instance, NR supplementation in preclinical studies has been shown to reduce chemotherapy-induced peripheral neuropathy,¹⁸ inhibit cancer metastasis,³⁵ and, in some cases, enhance tumor-suppressive effects.³⁶

A brief summary of these findings can be found below in the Appendix in Table 1, illustrating that NAD+ metabolism is complex and may be protective under certain conditions. Some researchers have even proposed that low NAD+ levels could be a risk factor for cancer,³⁷ highlighting that maintaining or restoring NAD+ may be beneficial rather than harmful.

Taken together, the current body of clinical and preclinical evidence indicates that increasing NAD+ levels through supplementation is not linked to cancer in humans. While research is ongoing and the field continues to evolve, there is no substantiated evidence that NAD+ precursors initiate or promote cancer in humans.

Media Misrepresentations of the Relationships Between NAD+ and Cancer

Sensationalized media coverage linking NAD+ to cancer has repeatedly created public confusion and alarm, often overstating preliminary or unrelated findings. Headlines and press releases have a tendency to imply causal relationships that are not supported by scientific evidence, so it’s essential to distinguish between early preclinical findings and meaningful human implications.

A notable example is the previously mentioned Maric et al., 2022 study¹² and the accompanying University of Missouri press release from November 2022. The press release headline suggested that NR supplementation “causes cancer risk and brain metastasis,” a claim that was not supported by the study itself. The experiment was a small, preclinical investigation using immunocompromised (“nude”) mice injected with aggressive, genetically engineered cancer cells—conditions that do not reflect human biology or real-world supplement use.

Dr. Carles Canto, a co-author and leading NAD+ researcher, criticized the headline as “clickbait” and scientifically inaccurate, stating,

“Thanks for the interest in that work. The title of the news article "Popular Dietary Supplement Causes Cancer Risk and Brain Metastasis" is clickbait material and totally inaccurate from a scientific standpoint. The experiment in Maric et al. does not allow this conclusion.”

Overall, the findings from Maric et al. were preliminary and do not support conclusions about cancer risk in humans. When placed in the context of the broader evidence, multiple preclinical studies indicate that NAD+ precursor supplementation can be beneficial in cancer-related contexts—such as reducing chemotherapy-induced peripheral neuropathy—without promoting tumor growth (see Table 1 for examples).

Additional context comes from Jiang et al., 2023,³⁶ who investigated NMN supplementation in triple-negative breast cancer (TNBC) models. TNBC is an aggressive and difficult-to-treat form of breast cancer. In this study, NMN reduced tumor growth and metastasis, suppressed lung metastasis, and improved overall survival in immunodeficient mice.³⁶

While both Jiang et al. and Maric et al. used TNBC models, their methods differed: Maric et al. injected tumor cells subcutaneously, whereas Jiang et al. injected cells into the inguinal mammary fat pad, better reflecting human breast cancer development. These methodological differences likely explain the contradictory results and highlight the need for careful interpretation. Importantly, the protective effects observed in the Jiang study highlight a more nuanced interpretation than that presented in the Maric press release, which may have overstated preliminary findings.

A second example involves Alzheimer’s-focused research examining NAD+ disruption in neurodegeneration. In this study by Chaubey et al., 2025, the pharmacological NAMPT activator P7C3-A20 restored NAD+ balance and improved neurological outcomes.³⁸ Although the study did not investigate cancer, a press release nonetheless reported:

“Dr. Pieper emphasized that currently available over-the-counter NAD+ precursors have been shown in animal models to raise cellular NAD+ to dangerously high levels that promote cancer.”

This conclusion extrapolates beyond the published findings and lacks support from human clinical evidence. Moreover, if supraphysiologic NAD+ (amounts greater than what’s typically found in the body) were inherently dangerous, the concern would apply equally to P7C3-A20 or other NAD-raising compounds. To date, no clinical studies suggest that NAD+ precursors increase cancer risk in humans.

These examples illustrate a broader problem: fear-based messaging can distort scientific discourse and misinform public health decisions. Claims about NAD+ and cancer derived from unrelated disease models, speculative statements, or preliminary preclinical data should not be extrapolated to humans, unless they are supported by translational studies. Accurate communication requires context, proportionality, and alignment with the actual scope of research.

Currently, there is no evidence from human studies that NAD+ precursor supplementation causes harm or increases cancer risk. While ongoing research is essential to fully understand NAD+ biology and its clinical implications, conclusions should not be drawn prematurely. Careful interpretation, transparency, and continued monitoring of scientific findings are necessary to maintain an accurate understanding of the relationship between NAD+ and human health.

Conclusion: Separating Fact from Fiction on NAD+ and Cancer

NAD+ supplementation has grown in popularity, sparking both consumer interest and concern about its potential links to cancer. However, it’s important to remember that cancer is a complex, multifactorial disease, primarily driven by genetic mutations, environmental exposures, and lifestyle factors—not the availability of NAD+. Like all cells, cancer cells rely on NAD+ for their growth and survival, but this does not mean NAD+ causes cancer.

Preclinical studies on NAD+ and cancer are often misinterpreted, and media coverage can exaggerate preliminary or unrelated findings, creating confusion. In contrast, human clinical evidence—including decades of research on NAD+ precursors like niacin, nicotinamide, NR, and NMN—has found no association with increased cancer risk. In fact, some preclinical studies even show a protective effect of NAD+ on certain cancer conditions.

Claims that NAD+ is inherently harmful are not supported by human evidence and must be understood within the proper scientific context. Accurate communication about NAD+ research is essential, given the molecule’s biological importance and the sensitivity of cancer discussions. Ongoing research and careful monitoring will continue to clarify the effects of NAD+ supplementation on human health.

Overall, NAD+ is essential for cellular health, and current evidence shows no harm from supplementation in humans. At the same time, continued research and nuanced understanding remain critical to fully uncover its role in health and disease, including cancer.

Appendix

Table 1. Preclinical Evidence of Beneficial Effects of NAD+ Precursors on Cancer and Related Conditions

Publication	Key Outcomes	Author Comments
Toth 1983 Lack of Carcinogenicity of Nicotinamide and Isonicotinamide Following Lifelong Administration to Mice Precursor(s): Nicotinamide & Isonicotinamide	Lifetime administration of nicotinamide or isonicotinamide at 1% concentrations in drinking water did not increase cancer incidence or reduce survival in Swiss mice, indicating that neither compound exhibited carcinogenic activity.	"...When NA was given intraperitoneally to male Holtzman rats in an earlier study, it resulted in no detectable carcinogenic action. Thus, the presently obtained negative results in mice, to some extent, corroborate the findings of previous investigators."
Santidrian et al., 2013 Mitochondrial Complex I Activity and NAD+/NADH Balance Regulate Breast Cancer Progression Precursor(s): Niacin (Nicotinic Acid) & Nicotinamide	Lowering NAD+ levels made breast cancer cells (MDA-MB-435 and MDA-MB-231) more aggressive and increased metastasis. Increasing NAD+ levels via niacin or nicotinamide inhibited experimental metastasis in xenograft models, reduced spontaneous metastasis, improved survival, and slowed disease progression across multiple breast cancer models. Nicotinamide prevented the progression of metastatic breast cancer in a transgenic mouse model that is known to emulate the human disease.	"...a combination of standard therapy with NAD+ precursor treatment may halt breast cancer progression and prevent relapse."
Tummala et al., 2014 Inhibition of De Novo NAD+ Synthesis by Oncogenic URI Causes Liver Tumorigenesis through DNA Damage Precursor(s): Nicotinamide Riboside	NR supplementation increased liver and pancreatic NAD+ levels. NR prevented pre-cancerous lesions, tumor formation, and overall cancer development by improving DNA repair. NR also reduced fibrosis and abnormal tumor-related signaling. In mice with fully developed liver tumors, prolonged NR treatment induced tumor regression and promoted tumor cell death.	"Therapies increasing NAD+ levels (e.g., NR) can be used to prevent HCC and cancers resulting from oncogene-induced DNA damage, but it remains to be determined whether boosting NAD+ is also therapeutic in nongenotoxic cancers." "...the development of more efficient and stable NAD+ boosters could provide therapies to prevent or cure cancers and associated metabolic dysfunctions."
Hamity et al., 2017 Nicotinamide Riboside, A Form of Vitamin B3 and NAD+ Precursor, Relieves the Nociceptive and Aversive Dimensions of Paclitaxel-Induced Peripheral Neuropathy in Female Rats Precursor(s): Nicotinamide Riboside	NR increased blood NAD+ levels by 50%, prevented neuropathy, and reversed paclitaxel-induced tactile hypersensitivity, without causing side effects or interfering with chemotherapy treatment.	"The ability of NR to reverse established tactile hypersensitivity and blunt PEAP [place avoidance/escape paradigm] behaviors suggests that it may be of benefit to a subset of those 30% of cancer survivors who continue to experience CIPN [chemotherapy-induced peripheral neuropathy] after chemotherapy has ended."
Yu et al., 2020 Disturbed Mitochondrial Dynamics in CD8+ TILS Reinforce T Cell Exhaustion Precursor(s): Nicotinamide Riboside	NR improved mitochondrial health and fitness in CD8+ T cells by reducing damaged mitochondria and lowering mitochondrial oxidative stress. In tumor-bearing mice, NR increased T cell numbers, slowed melanoma and colon tumor growth, and further enhanced the efficacy of immunotherapy when used in combination.	"...melanoma and colon tumor growth was significantly impeded in NR-fed mice, and combined treatment with the NR diet and immune checkpoint blockade elicited additive antitumor responses…" "Collectively, these findings reveal that supplementation with NR alleviates mitochondrial dysfunction and further induces additive antitumor immunity in conjunction with immune check-point blockade treatments."
Scatozza et al., 2020 Nicotinamide Inhibits Melanoma In Vitro and In Vivo Precursor(s): Nicotinamide	Nicotinamide strongly inhibited melanoma growth by increasing cell death, blocking cell-cycle progression, and increasing NAD+ and energy levels in tumor cells. In mice, nicotinamide slowed tumor growth, improved survival, and enhanced anti-tumor immunity.	"The current study presents for the first time strong in vitro and in vivo anti-melanoma activity of NAM and several data indicating the underlying molecular mechanisms."
Hamity et al., 2020 Nicotinamide Riboside Relieves Paclitaxel-Induced Peripheral Neuropathy and Enhances Suppression of Tumor Growth in Tumor-Bearing Rats Precursor(s): Nicotinamide Riboside	NR supplementation reduced the loss of intraepidermal nerve fibers (IENF) in paclitaxel-treated rats that both did and did not have tumors. In tumor-bearing rats, NR also reduced hypersensitivity to touch and cold caused by paclitaxel. Importantly, NR did not promote cancer growth and instead enhanced the tumor-suppressing effects of paclitaxel.	"Transition of this work to tumor-bearing rats reaffirmed the ability of NR to suppress the somatosensory and affective sequelae of paclitaxel while addressing potential concerns of NR's effect on tumor growth. It also revealed an intriguing finding that NR may cooperate with paclitaxel to suppress tumor growth in vivo."
Park et al., 2021 Nicotinamide Riboside Vitamin B3 Mitigated C26 Adenocarcinoma–Induced Cancer Cachexia Precursor(s): Nicotinamide Riboside	An NR-supplemented diet reduced cancer cachexia (muscle wasting) in a mouse model by preserving thigh and calf muscle mass, preventing fat loss, and improving the expression of genes involved in muscle maintenance and metabolism.	"...our investigation revealed that preemptive and dietary intake of NR in patients at high risk of developing cancer cachexia can be a potential regimen to inhibit the occurrence of a catabolic catastrophe, cachexia inflammation, and muscle atrophy."
Acklin et al., 2022 Nicotinamide Riboside Alleviates Cisplatin-Induced Peripheral Neuropathy via SIRT2 Activation Precursor(s): Nicotinamide Riboside	NR prevented and alleviated cisplatin-induced peripheral neuropathy in mice by increasing NAD+ and activating SIRT2-dependent nerve protection, without compromising cisplatin's anticancer activity.	"NR may provide increased protection from cancer treatment toxicity in select patients or clinical settings, and NAD+ expression could act as a predictive marker for toxicity risk and chemotherapy response."
Jiang et al., 2023 NAD+ Supplementation Limits Triple-Negative Breast Cancer Metastasis via SIRT1-P66Shc Signaling Precursor(s): Nicotinamide Mononucleotide	NMN supplementation reduced the growth and metastasis of triple-negative breast cancer (TNBC) in immunodeficient mice. NMN also suppressed tumor metastasis to the lung and improved the overall survival of the tumor-bearing mice.	"...our study identifies that NAD+ supplementation suppresses TNBC progression and cell migration and invasion." "These findings provide evidence for serving SIRT1 as a tumor suppressor gene and indicate the great potential of NAD+ booster supplements to improve the clinical therapeutic effects of TNBC."
Pang et al., 2023 Nicotinamide Adenine Dinucleotide Precursor Suppresses Hepatocellular Cancer Progression in Mice Precursor(s): Nicotinamide Riboside	NR supplementation increased NAD+ levels, reduced tumor growth and metastasis, alleviated cancer-induced weight loss, and improved survival in mouse models of hepatocellular carcinoma, while inhibiting cancer cell migration and invasion in vitro (cells).	"In summary, we found that replenishing NAD pools by NR could inhibit tumor growth and cancer metastasis as well as promote the overall health status of tumor-bearing mice. Our study revealed that boosting NAD by NR supplementation could be a novel strategy for the prevention of HCC progression."
Wu et al., 2025 Nicotinamide Riboside Enhances the Efficacy of Gemcitabine and Suppresses PDAC Premalignant Lesions via SIRT3 Activation Precursor(s): Nicotinamide Riboside	NR activated SIRT3 to delay pancreatic cancer progression and enhance gemcitabine chemotherapy, suppressing tumor growth and overcoming therapeutic resistance in preclinical models.	"These findings establish NR as a promising SIRT3-targeting adjuvant that both enhances the efficacy of standard chemotherapy and delays carcinogenesis, thereby overcoming therapeutic resistance in established PDAC and potentially impeding its development."

Disclaimer: This article is for informational purposes only and is not a substitute for professional medical advice. Always consult your healthcare provider before starting, stopping, or changing any supplement regimen or treatment. The content here does not constitute personalized medical guidance.

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