Formulated to the species.
Dosed to the research.

Is NMN safe for pets?

The primary canine-specific safety reference is a 2020 study published in Frontiers in Pharmacology (You et al., "Subacute Toxicity Study of Nicotinamide Mononucleotide via Oral Administration"). This study specifically tested oral NMN administration in beagle dogs over 14 days at high doses, finding that NMN was well tolerated with no adverse clinical symptoms — no vomiting, diarrhoea, or lethargy. At the highest doses tested, only mild and transient increases in creatinine and uric acid were observed, while liver function markers remained unaffected. The study concluded that oral NMN has mild or minimal adverse effects and established a reference dose range for safe oral administration. It is important to note that the doses used in this study were substantially higher than typical supplemental doses — which provides a useful safety margin under real-world conditions.

Separately, a 2024 study published in Aging Cell (Zeng et al.) administered NMN to aged dogs as one of several interventions in a controlled study examining anti-ageing approaches in canine subjects. NMN was well tolerated across the treatment period, and the study identified measurable reductions in inflammatory markers IL-6 and TNF-α in treated dogs.

Two further peer-reviewed toxicology studies reinforce the safety picture, conducted in rats under rigorous OECD guidelines. Cros et al. (2021), published in Food and Chemical Toxicology, evaluated NMN over a 90-day sub-chronic oral administration period and found it was not mutagenic or genotoxic, with a No-Observable Adverse Effect Level (NOAEL) established at or above 1,500 mg/kg/day. A second 90-day rat study, Yu et al. (2024) in Current Research in Toxicology, similarly found NMN non-mutagenic, with an acute oral LD50 greater than 2,000 mg/kg body weight. While these studies were conducted in rats rather than dogs or cats, they provide important supporting evidence on the general toxicological profile of NMN at sustained doses.

On kidney function specifically: the mild creatinine elevation observed in the 2020 beagle study occurred only at very high doses and was not considered clinically significant in the healthy dogs studied. However, pets with pre-existing kidney disease represent a different risk profile from those in safety studies, and any supplement that may influence renal markers warrants veterinary oversight in those animals. Similarly, dogs on long-term medication or with complex health conditions should be assessed by a vet before starting NMN supplementation.

Likewise for cats, vet involvement is particularly important for cats with kidney disease, liver conditions, or those on ongoing medication.

As with any supplement, some dogs and cats may experience mild digestive adjustment when NMN is first introduced. If vomiting, diarrhoea, or lethargy persists beyond the first few days, we recommend discontinuing use and consulting your vet.

Heart Health

Mitochondrial decline is a key factor in heart disease. A 2017 study, “Short-term administration of Nicotinamide Mononucleotide preserves cardiac mitochondrial homeostasis and prevents heart failure”, found that NMN supported mitochondrial function and helped protect against heart failure in mice. While the work was conducted in rodents, the mechanisms involved — mitochondrial stability and energy production — are highly relevant to canine heart health.

Vascular Function

Vascular aging is linked to stiffness, oxidative stress, and poor circulation. In a 2016 paper published in Aging Cell, “Nicotinamide mononucleotide supplementation reverses vascular dysfunction and oxidative stress with aging in mice”, NMN was shown to restore vascular elasticity and reduce oxidative stress. A separate 2020 toxicity study also observed lower blood lipid levels, including total cholesterol and triglycerides, in animals supplemented with NMN — both of which contribute to healthier cardiovascular function.

Metabolic Support & Diabetes

Metabolic decline is a hallmark of aging in both humans and pets. A 2011 study, “Nicotinamide mononucleotide, a key NAD⁺ intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice”, reported that NMN improved insulin sensitivity and glucose tolerance. These findings suggest NMN could have a role in supporting pets with age- or diet-related glucose regulation challenges.

Cognitive Function & Aging

Oxidative stress and mitochondrial dysfunction are also central to age-related cognitive decline. In a 2017 study, “Nicotinamide mononucleotide inhibits JNK activation to reverse Alzheimer disease”, NMN supplementation improved cognition and reduced amyloid plaque burden in mice. This, combined with evidence from the 2018 review “Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence” (Rajman, Chwalek & Sinclair), highlights NMN’s broader role in maintaining NAD⁺ levels and potentially slowing aspects of neurological aging — making it an intriguing candidate for supporting pets with cognitive decline.

• A study feeding GLM-supplemented diet for 45 days to dogs with arthritis showed clinical improvements in signs such as pain, swelling, and crepitus versus baseline.
• In a blinded placebo-controlled trial (101 dogs) using a combination of GLM + krill oil extracts (EAB-277) vs NSAIDs/other extracts, GLM combination delivered significant pain relief in dogs with hip osteoarthritis.
• In cats, Lascelles et al. (2010, Journal of Veterinary Internal Medicine) evaluated a therapeutic diet containing green lipped mussel extract alongside EPA/DHA and glucosamine/chondroitin in cats with degenerative joint disease. Cats on the diet became more active than those on a control diet.

Palmitoylethanolamide (PEA) is an endogenous fatty acid amide from the ALIAmide family, produced by the body on demand in response to tissue stress. It acts on the nuclear receptor PPAR-α and down-regulates mast cell activation, helping resolve the local inflammatory signalling behind discomfort rather than masking it.

• A review by Petrosino & Di Marzo (2017, British Journal of Pharmacology) summarised PEA's pharmacology and the first clinical data on its newer, better-absorbed formulations.
• In cats, a pilot study by Scarampella et al. (2001, Veterinary Dermatology) evaluated a PEA analogue in cats with eosinophilic granuloma and eosinophilic plaque, both mast cell–driven inflammatory conditions.
• PEA's absorption depends heavily on particle size and delivery form, which is why formulation matters as much as dose for this ingredient.

Undenatured type II collagen is processed at low temperatures so it keeps its native triple-helix structure. Rather than acting as a building block, it works through oral tolerance: intact collagen is recognised by immune tissue in the gut (Peyer's patches), which signals regulatory T cells to help moderate the immune activity that contributes to cartilage breakdown. That's why it works at small daily doses.

• Deparle et al. (2005, Journal of Veterinary Pharmacology and Therapeutics) reported reduced pain and improved mobility in arthritic dogs given undenatured type II collagen.
• Gupta et al. (2012, Journal of Animal Physiology and Animal Nutrition) compared undenatured type II collagen with glucosamine and chondroitin in arthritic dogs, measuring pain objectively with a ground force plate.

Cats have very limited ability to synthesise taurine and rely on it exclusively to conjugate bile acids, creating a continuous daily loss that must be replaced through diet.

• Pion et al. (1987, Science) identified low plasma taurine as a cause of dilated cardiomyopathy in cats, and showed the heart muscle dysfunction was reversible with taurine supplementation. This finding changed how commercial cat food is formulated worldwide.
• Hayes, Carey & Schmidt (1975, Science) linked taurine deficiency in cats to retinal degeneration, establishing taurine's role in feline eye health.

L-Carnitine shuttles long-chain fatty acids into mitochondria via the carnitine palmitoyltransferase system, where they're burned for energy.

• Center et al. (2000, Journal of Veterinary Internal Medicine) studied oral L-carnitine in obese pet cats undergoing rapid weight loss, examining its influence on weight loss and liver fat metabolism.
• By supporting efficient fat metabolism, L-carnitine helps cats draw energy from fat stores while sparing lean muscle, which is especially relevant as muscle mass declines with age.

Vitamin B12 (cobalamin) is a cofactor for methionine synthase and methylmalonyl-CoA mutase, enzymes essential for methylation and for turning fats and proteins into usable energy. It also supports nerve function and red blood cell formation.

• Ruaux, Steiner & Williams (2005, Journal of Veterinary Internal Medicine) documented the early biochemical and clinical responses to cobalamin supplementation in cats with low B12 status.
• Senior cats are prone to lower cobalamin status as intestinal absorption becomes less efficient with age.

• Trials using glucosamine in canine osteoarthritis show measurable improvements in comfort, reduced lameness, especially in mild-to-moderate cases.
• Other studies show slower progression of cartilage damage / symptoms when glucosamine + chondroitin are used as adjuncts to diet / other therapies.

Boswellia serrata is rich in AKBA (acetyl-11-keto-β-boswellic acid), a compound known to inhibit the 5-LOX enzyme involved in chronic inflammation. In a 2004 veterinary study, “Dietary support with Boswellia resin in canine inflammatory joint and spinal disease” (Reichling et al., Schweizer Archiv für Tierheilkunde), 71% of dogs showed improvement in signs such as lameness and stiffness after just two weeks of a six-week supplementation trial.

Additional research in mammalian models supports these outcomes, with boswellic acids shown to reduce cartilage-degrading enzymes (MMPs) and calm joint inflammation. Together, these findings underline Boswellia’s capacity to support joint comfort and easier movement in dogs experiencing age- or activity-related stiffness.

Curcumin is notoriously difficult for mammals to absorb, which is why we use the phytosome form (curcumin bound to phospholipids), designed to dramatically improve bioavailability compared with raw turmeric.

• In a randomised, double-blind, placebo-controlled study, Innes et al. (2003, Veterinary Record) evaluated a turmeric extract in dogs with osteoarthritis, with veterinary assessments favouring the treated group.
• Colitti et al. (2012, Veterinary Immunology and Immunopathology) found dietary curcumin produced anti-inflammatory changes in gene expression in the white blood cells of dogs with osteoarthritis.

Mechanistically, curcumin modulates inflammatory pathways such as COX-2, NF-κB and oxidative stress markers — the same pathways implicated in canine osteoarthritis.

• Omega-3 fatty acids in fish oil have been shown to reduce joint pain and improve mobility in dogs with osteoarthritis, particularly when combined with other joint support agents.
• In dogs with osteoarthritis, fish oil improved weight bearing and reduced inflammation per owner assessments and objective gait analysis.

While fish oil’s EPA and DHA are clinically shown to support joint comfort, pets require meaningful amounts — typically in the grams, not milligrams — to see real benefits. Most pet supplements include only 100–500 mg of fish oil, far below therapeutic levels. Pawever Plus for Dogs includes a moderate amount for its heart and brain support, and our cat formula leaves it out entirely. For a full clinical dose of EPA + DHA, we recommend Pawever Omega Oil alongside Pawever Plus.

• Studies in dogs post-joint injury or surgery show that HA supplementation supports improved biomarkers of cartilage metabolism and helps recovery.
• Specifically, in dogs with knee surgery (cranial cruciate ligament rupture, TTA), oral HA improved biomarkers of osteoarthritis over 10 weeks (increases in HA, decreases in inflammation markers).

Coenzyme Q10 is embedded in the inner mitochondrial membrane, where it carries electrons between complexes of the electron transport chain to produce ATP. In its reduced form it is also a lipid-phase antioxidant that protects cell membranes and helps regenerate vitamin E.

• Crane (2001, Journal of the American College of Nutrition) reviewed CoQ10's biochemical functions in energy production and antioxidant protection.
• Tissues with the highest energy demands, particularly heart muscle, rely most on CoQ10, and the body's own production declines with age. Most clinical research to date has been conducted in humans and other mammals.

• Studies in dogs show that Vitamin E, especially in combination with other antioxidants, helps reduce biomarkers of oxidative stress in aging or joint-stressed animals.
• Diets enriched with vitamins E, C, and β-carotene reduced markers of oxidative damage. Animals fed these diets showed increased antioxidant capacity and less cellular degradation.

• Animal nutrition research and guideline-reviews consistently show that manganese deficiency impairs cartilage health and slows soft-tissue repair, while balanced manganese intake helps support joint resilience, metabolic function, and antioxidant defense.