|Preferred IUPAC name
3D model (JSmol)
CompTox Dashboard (EPA)
|Molar mass||123.111 g·mol−1|
|Appearance||White, translucent crystals|
|Density||1.473 g cm−3|
|Melting point||237 °C; 458 °F; 510 K|
|18 g L−1|
|Acidity (pKa)||2.0, 4.85|
Refractive index (nD)
Std enthalpy of
|−344.9 kJ mol−1|
Std enthalpy of
|−2.73083 MJ mol−1|
|C04AC01 (WHO) C10BA01 (WHO) C10AD02 (WHO) C10AD52 (WHO)|
|Intramuscular, by mouth|
|GHS Signal word||Warning|
|P264, P280, P305+351+338, P337+313, P501|
|NFPA 704 (fire diamond)|
|Flash point||193 °C (379 °F; 466 K)|
|365 °C (689 °F; 638 K)|
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
|what is ?)(|
|CompTox Dashboard (EPA)|
Niacin, also known as nicotinic acid, is an organic compound and a form of vitamin B3, an essential human nutrient. Niacin is obtained in the diet from a variety of whole and processed foods, with highest contents in fortified packaged foods, meat, poultry, red fish such as tuna and salmon, lesser amounts in nuts, legumes and seeds. Niacin as a dietary supplement is used to treat pellagra, a disease caused by niacin deficiency. Signs and symptoms include skin and mouth lesions, anemia, headaches, and tiredness. Many countries require its addition to wheat flour or other food grains, thereby reducing the risk of pellagra.
Niacin is also a prescription medication. Amounts far in excess of the recommended dietary intake for vitamin functions will lower blood triglycerides and low density lipoprotein cholesterol (LDL-C), and raise blood high density lipoprotein cholesterol (HDL-C, often referred to as "good" cholesterol). There are two forms: immediate-release and sustained-release niacin. Initial prescription amounts are 500 mg/day, increased over time until a therapeutic effect is achieved. Immediate-release doses can be as high as 3,000 mg/day; sustained-release as high as 2,000 mg/day. Despite the proven lipid changes, niacin has not been found useful for decreasing the risk of cardiovascular disease in those already on a statin. A 2010 review had concluded effectiveness of niacin as a mono-therapy, but a 2017 review incorporating twice as many trials concluded that prescription niacin, while affecting lipid levels, did not reduce all-cause mortality, cardiovascular mortality, myocardial infarctions, nor fatal or non-fatal strokes. Prescription niacin was shown to cause hepatotoxicity and increase risk of type 2 diabetes. Niacin prescriptions in the U.S. had peaked in 2009, at 9.4 million, declining to 1.3 million by 2017.
Although niacin and nicotinamide (niacinamide) are identical in their vitamin activity, nicotinamide does not have the same pharmacological, lipid-modifying effects or side effects as niacin, i.e., when niacin takes on the -amide group, it does not reduce cholesterol nor cause flushing.
Treatment of deficiency
Niacin and niacinamide are used for prevention and treatment of pellagra, a disease caused by lack of the vitamin. For treating deficiency, the World Health Organization (WHO) recommends administering niacinamide instead of niacin, to avoid the flushing side effect commonly caused by niacin. Guidelines suggest using 300 mg/day for three to four weeks. Dementia and dermatitis show improvement within a week. Because deficiencies of other B-vitamins may be present, the WHO recommends a multi-vitamin in addition to the niacinamide.
Prescription niacin, in immediate-release and slow-release forms, is used to treat primary hyperlipidemia and mixed dyslipidemia. It is used either as a monotherapy or in combination with other lipid-modifying drugs. Dosages start at 500 mg/day and are often gradually increased to as high as 3000 mg/day for immediate release or 2000 mg/day for slow release (also referred to as sustained release) to achieve the targeted lipid changes (lower LDL-C and triglycerides, and higher HDL-C). Prescriptions in the U.S. peaked in 2009, at 9.4 million and had declined to 1.3 million by 2017. Systematic reviews found no effect of prescription niacin on all-cause mortality, cardiovascular mortality, myocardial infarctions, nor fatal or non-fatal strokes despite raising HDL cholesterol. Reported side effects include an increased risk of diabetes.
Extended release niacin was combined with lovastatin as a prescription drug combination (trade name Advicor) for the treatment of dyslipidemia. It was a combination of the vitamin niacin in extended release form and the statin drug lovastatin (trade name Mevacor). The combination preparation was developed by Kos Pharmaceuticals, Inc., which was acquired by Abbott Laboratories in 2006, subsequently transferred to AbbVie Inc. when that company was spun off from Abbott in 2013. Advicor was approved by the U.S. Food and Drug Administration (FDA) on December 17, 2001. Similarly, an Abbott Laboratories combination drug (trade name Simcor) consisting of an extended release form of the vitamin and the statin drug simvastatin was approved by the FDA on February 15, 2008. The FDA withdrew approval of both drugs on 18 April 2016. The reason given: "Based on the collective evidence from several large cardiovascular outcome trials, the Agency has concluded that the totality of the scientific evidence no longer supports the conclusion that a drug-induced reduction in triglyceride levels and/or increase in HDL-cholesterol levels in statin-treated patients results in a reduction in the risk of cardiovascular events." AbbVie Inc. agreed to voluntarily discontinue marketing Advicor and Simcor.
Prescription immediate release (Niacor) and extended release (Niaspan) niacin are contraindicated with active liver disease, persistent elevated serum transaminases, active peptic ulcer disease, or arterial bleeding. Also contraindicated for women who are pregnant or expecting to become pregnant, or are lactating.
The most common adverse effects of niacin at (50–500 mg) are flushing (e.g., warmth, redness, itching or tingling), headache, abdominal pain, diarrhea, dyspepsia, nausea, vomiting, rhinitis, pruritus and rash. These can be minimized by initiating therapy at low dosages, increasing dosage gradually, and avoiding administration on an empty stomach.
The acute adverse effects of high-dose niacin therapy (1–3 grams/day) – which is commonly used in the treatment of hyperlipidemias – further include hypotension, fatigue, glucose intolerance and insulin resistance, heartburn, blurred or impaired vision, and macular edema. With long-term use, the adverse effects of high-dose niacin therapy also include hepatic dysfunction (associated with fatigue, nausea, and loss of appetite), hepatitis, and acute liver failure; these hepatotoxic effects of niacin occur more often when extended-release dosage forms are used. The long-term use of niacin at high doses (2 grams/day) also significantly increases the risk of cerebral hemorrhage, ischemic stroke, gastrointestinal ulceration and bleeding, diabetes, dyspepsia, and diarrhea.
Flushing usually lasts for about 15 to 30 minutes, though it can sometimes last up to two hours. It is sometimes accompanied by a prickly or itching sensation, in particular, in areas covered by clothing. Flushing can be blocked by taking 300 mg of aspirin half an hour before taking niacin, by taking one tablet of ibuprofen per day or by co-administering the prostaglandin receptor antagonist laropiprant. Taking niacin with meals also helps reduce this side effect. Acquired tolerance will also help reduce flushing; after several weeks of a consistent dose, most patients no longer experience flushing. Reduction of flushing focuses on altering or blocking the prostaglandin-mediated pathway. Slow- or "sustained"-release forms of niacin have been developed to lessen these side effects.
Prostaglandin (PGD2) is the primary cause of the flushing reaction, with serotonin appearing to have a secondary role in this reaction. The effect is mediated by prostaglandin E2 and D2 due to GPR109A activation of epidermal Langerhans cells and keratinocytes. Langerhans cells use cyclooxygenase type 1 (COX-1) for PGE2 production and are more responsible for acute flushing, while keratinocytes are COX-2 dependent and are in active continued vasodilation. Flushing was often thought to involve histamine, but histamine has been shown not to be involved in the reaction.
Niacin in medicinal doses causes elevation in serum aminotransferase in some people. The reaction is asymptomatic and usually resolves even when the drug intakes continues. The effect is dose-related. At higher doses - above three grams per day - there can also be a decrease in coagulation factors and an increase in bleeding and bruising. These changes revert to normal when therapy is stopped. Niacin can also cause serious hepatotoxicity. This is uncommon, and more likely with the sustained release form of the product versus immediate release. Onset is days to weeks. Early symptoms include nausea, vomiting and abdominal pain, followed by jaundice and pruritus. Serum aminotransferase concentration is very high. The mechanism is thought to be toxicity of elevated serum niacin. Lowering dose or switching to the immediate release form can resolve symptoms. In rare instances the injury is severe, and progresses to liver failure.
The high doses of niacin used to improve the lipid profile have been shown to elevate fasting blood glucose in people with type 2 diabetes. Reviews reported that long-term niacin therapy was also associated with an increase in the risk of new-onset type 2 diabetes.
Side effects of heart arrhythmias have also been reported.[page needed] Increased prothrombin time and decreased platelet count have been reported; therefore, these should be monitored closely in patients who are also taking anticoagulants. Extremely high doses of niacin can also cause niacin maculopathy, a thickening of the macula and retina, which leads to blurred vision and blindness. This maculopathy is reversible after niacin intake ceases.
Plasma concentrations of other niacin metabolites and of niacin are not useful markers of niacin status. Urinary excretion of the methylated metabolite N1-methyl-nicotinamide is considered reliable and sensitive. The measurement requires a 24-hour urine collection. For adults, a value of less than 5.8 µmol/day represent deficient niacin status and 5.8 to 17.5 µmol/day represents low. An alternative mean of expressing urinary N1-methyl-nicotinamide is as mg/g creatinine in a 24-hour urine collection, with deficient defined as <0.5, low 0.5-1.59, acceptable 1.6-4.29, and high >4.3 Niacin deficiency occurs before the signs and symptoms of pellagra appear. Erythrocyte nicotinamide adenine dinucleotide (NAD) concentrations potentially provides another sensitive indicator of niacin depletion, although definitions of deficient, low, etc. have not been established. Lastly, plasma tryptophan decreases on a low niacin diet because tryptophan converts to niacin. However, low tryptophan could also be caused by a diet low in this essential amino acid.
Between 1906 and 1940 more than three million Americans were affected by pellagra, with more than 100,000 deaths. Joseph Goldberger was assigned to study pellagra by the Surgeon General of the United States and produced good results in diet studies conducted at orphanages. In the late 1930s, studies by Tom Douglas Spies, Marion Blankenhorn, and Clark Cooper established that niacin cured pellagra in humans. The prevalence of the disease was greatly reduced as a result.
Niacin deficiency is rarely seen in developed countries, and it is more typically associated with poverty, malnutrition or chronic alcoholism. It also tends to occur in less developed areas where people eat maize (corn) as a staple food, as maize is the only grain low in digestible niacin. A cooking technique called nixtamalization i.e., pretreating with alkali ingredients, increases the bioavailability of niacin during maize meal/flour production. For this reason, people who consume corn as tortillas or hominy are not at risk of niacin deficiency.
Severe deficiency of niacin in the diet causes the disease pellagra, which is characterized by diarrhea, sun-sensitive dermatitis, and dementia, hyperpigmentation, thickening of the skin, inflammation of the mouth and tongue, digestive disturbances, amnesia, delirium, and eventually death, if left untreated. Common psychiatric symptoms of niacin deficiency include irritability, poor concentration, anxiety, fatigue, restlessness, apathy, and depression. Chronic alcoholism combined with niacin deficiency may lead to psychiatric symptoms reversible with niacin supplementation.
Hartnup disease is a hereditary nutritional disorder resulting in niacin deficiency. This condition was first identified in the 1950s by the Hartnup family in London. It is due to a deficit in the intestines and kidneys, making it difficult for the body to break down and absorb dietary tryptophan (an essential amino acid that is utilized to synthesize niacin). The resulting condition is similar to pellagra, including symptoms of red, scaly rash, and sensitivity to sunlight. Oral niacin is given as a treatment for this condition in doses ranging from 40–200 mg, with a good prognosis if identified and treated early. Niacin synthesis is also deficient in carcinoid syndrome, because of metabolic diversion of its precursor tryptophan to form serotonin.
Niacin is found in a variety of whole and processed foods, including fortified packaged foods, meat from various animal sources, seafoods, and spices. In general, animal-sourced foods provide about 5-10 mg niacin per serving., although dairy foods and eggs have little. Some plant-sourced foods such as nuts and grains provide about 2-5 mg niacin per serving, although this naturally present niacin is largely bound to polysaccharides and glycopeptides, making it only about 30% bioavailable. Fortified food ingredients such as wheat flour have niacin added, which is bioavailable. Among whole food sources with the highest niacin content per 100 grams:
The U.S. Institute of Medicine (renamed National Academy of Medicine in 2015) updated Estimated Average Requirements (EARs) and Recommended Dietary Allowances (RDAs) for niacin in 1998 (see Table). The European Food Safety Authority (EFSA) refers to the collective set of information as Dietary Reference Values (DRV), with Population Reference Intake (PRI) instead of RDA, and Average Requirement instead of EAR. AI and UL defined the same as in United States. Units are milligrams per megajoule (MJ) of energy consumed. For women (including those pregnant or lactating), men and children the PRI is 1.6 mg per megajoule. As the conversion is 1 MJ = 238.8 kcal, an adult consuming 2388 calories should be consuming 16 mg niacin. This is comparable to U.S. RDAs (14 mg/day for adult women, 16 mg/day for adult men). The EFSA niacin UL is set at 10 mg/day, which is much less than the U.S. value. The UL applies to niacin as a supplement consumed as one dose, and in intended to avoid the skin flush reaction. This explains why the PRI can be higher than the UL.
Both the DRI and DRV describe amounts needed as niacin equivalents (NE), calculated as 1 mg NE = 1 mg niacin or 60 mg of the essential amino acid tryptophan. This is because the amino acid is utilized to synthesize the vitamin.
For U.S. food and dietary supplement labeling purposes the amount in a serving is expressed as a percent of Daily Value (%DV). For niacin labeling purposes 100% of the Daily Value is 16 mg. Prior to 27 May 2016 it was 20 mg, revised to bring it into agreement with the RDA. Compliance with the updated labeling regulations was required by 1 January 2020, for manufacturers with $10 million or more in annual food sales, and by 1 January 2021 for manufacturers with less than $10 million in annual food sales. During the first six months following the 1 January 2020 compliance date, the FDA plans to work cooperatively with manufacturers to meet the new Nutrition Facts label requirements and will not focus on enforcement actions regarding these requirements during that time. A table of the old and new adult Daily Values is provided at Reference Daily Intake.
(mg / 100g)
|Nutritional yeast per 2 Tbsp (16 g)||56|
|Tuna, light, canned||10.1|
|Turkey depending on what part, how cooked||7-12|
|Chicken depending on what part, how cooked||7-12|
(mg / 100g)
|Beef depending on what part, how cooked||4-8|
|Pork depending on what part, how cooked||4-8|
|Tuna, white, canned||5.8|
(mg / 100g)
|Potato, baked, with skin||1.4|
Vegetarian and vegan diets can provide adequate amounts if products such as nutritional yeast, peanuts, peanut butter, tahini, brown rice, mushrooms, avocado and sunflower seeds are included. Fortified foods and dietary supplements can also be consumed to insure adequate intake.
Niacin naturally found in food is susceptible to destruction from high heat cooking, especially in the presence of acidic foods and sauces. It is soluble in water, and so may also be lost from foods boiled in water.
The Food Fortification Initiative lists all countries in the world that conduct fortification programs, and within each country, what nutrients are added to which foods, and whether those programs are voluntary or mandatory. As of 2019, 53 countries required food fortification of wheat flour with niacin and 14 also mandate fortification of maize flour.
Niacin and nicotinamide are both precursors of the coenzymes nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP) in vivo. NAD converts to NADP by phosphorylation in the presence of the enzyme NAD+ kinase. NADP and NAD are coenzymes for many dehydrogenases, participating in many hydrogen transfer processes. NAD is important in catabolism of fat, carbohydrate, protein, and alcohol, as well as cell signaling and DNA repair, and NADP mostly in anabolism reactions such as fatty acid and cholesterol synthesis. High energy requirements (brain) or high turnover rate (gut, skin) organs are usually the most susceptible to their deficiency.
The lipid-therapeutic effects of niacin are partly mediated through the activation of G protein-coupled receptors, including niacin receptor 1 (NIACR1) and niacin receptor 2 (NIACR2) which are highly expressed in adipose tissue, spleen, immune cells, and keratinocytes, but not in other expected organs such as liver, kidney, heart or intestine. NIACR1 and NIACR2 inhibit cyclic adenosine monophosphate (cAMP) production and thus fat breakdown in adipose tissue and free fatty acids available for liver to produce triglycerides and very-low-density lipoproteins (VLDL) and consequently low-density lipoprotein (LDL). A decrease in free fatty acids also suppresses liver expression of apolipoprotein C3 and PPARg coactivator-1b, thus increasing VLDL turnover and reducing its production.
The mechanism behind niacin increasing HDL is not totally understood, but seems to occur in various ways. Niacin increases apolipoprotein A1 levels due to anticatabolic effects resulting in higher reverse cholesterol transport. It also inhibits HDL hepatic uptake, down-regulating production of the cholesterol ester transfer protein (CETP) gene. Finally, it stimulates the ABCA1 transporter in monocytes and macrophages and upregulates peroxisome proliferator-activated receptor gamma, resulting in reverse cholesterol transport.
Niacin reduces secondary outcomes associated with atherosclerosis, such as low-density lipoprotein cholesterol (LDL), very low-density lipoprotein cholesterol (VLDL-C), and triglycerides (TG), but increases high-density lipoprotein cholesterol (HDL). Other effects include anti-thrombotic and vascular inflammation, improving endothelial function, and plaque stability. As mediators produced from adipocytes, adipokines, such as tumor necrosis factor (TNF)-a, interleukins and chemokines, have pro-inflammatory effects, while others, such as adiponectin, have anti-inflammatory effects that influence the onset of atherosclerosis. Niacin also appears to upregulate brain-derived neurotrophic factor and tropomyosin receptor kinase B (TrkB) expression.
Research has been able to show the function of niacin in the pathway lipid metabolism. It is seen that this vitamin can decrease the synthesis of apoB-containing lipoproteins such as VLDL, LDL, IDL and lipoprotein (a) via several mechanisms: (1) directly inhibiting the action of DGAT2, a key enzyme for triglyceride synthesis; (2) influencing binding to the receptor HCAR2 thereby decreasing lipolysis and FFA flux to the liver for triglyceride synthesis; and (3) increasing apoB catabolism. HDL levels are increased by niacin through direct and indirect pathways, such as by decreasing cholesterylester transfer protein activity and triglyceride levels.
Both niacin and niacinamide are rapidly absorbed from the stomach and small intestine. Absorption is facilitated by sodium-dependent diffusion, and at higher intakes, via passive diffusion. Unlike some other vitamins, the percent absorbed does not decrease with increasing dose, so that even at amounts of 3-4 grams, absorption is nearly complete. Niacinamide is the major form in the bloodstream. In the liver, niacinamide is converted to storage nicotinamide adenine dinucleotide (NAD). As needed, liver NAD is hydrolyzed to niacinamide and niacin for transport to tissues, there reconverted to NAD to serve as an enzyme cofactor. Excess niacin is methylated in the liver to N1-methylnicotinamide (NMN) and excreted in urine as such or as the oxidized metabolite N1-methyl-2-pyridone-5-carboxamide (2-pyridone). Decreased urinary content of these metabolites is a measure of niacin deficiency.
In all animals the liver can synthesize niacin from the essential amino acid tryptophan, a five-step process with the penultimate compound being quinolinic acid (see figure). Some bacteria and plants utilize aspartic acid in a pathway that also goes to quinolinic acid. For humans, the efficiency of conversion is estimated as requiring 60 mg of tryptophan to make 1 mg of niacin. Riboflavin, vitamin B6 and iron are required for the process. The US Institute of Medicine set a Recommended Dietary Allowance (RDA) for adults of 5 mg/kg body weight/day for tryptophan, equivalent to 350 mg/day for a 70 kg (154 lb) adult. The RDA for protein is 0.8 g/kg, equivalent to 56 g/day for a 70 kg adult. Dietary protein is approximately 1% tryptophan, so achieving the RDA for protein contributes about 560 mg tryptophan per day. Pellagra, a disease due to niacin deficiency, was observed in Europe and elsewhere when poor people consumed large amounts of corn as part of their protein-poor diet, but not so for those in areas where wheat or rice were the low-cost grain, the reason being that corn protein has a lower tryptophan content.
Commercial production for animal feed and other purposes is of nicotinamide (niacinamide), which can be converted to niacin. Nicotinonitrile is produced by ammoxidation of 3-methylpyridine. Nitrile hydratase is then used to catalyze nicotinonitrile to nicotinamide. According to Ullmann's Encyclopedia of Industrial Chemistry, worldwide 31,000 tons of nicotinamide were sold in 2014.
Physical and chemical properties
This colorless, water-soluble solid is a derivative of pyridine, with a carboxyl group (COOH) at the 3-position. Other forms of vitamin B3 include the corresponding amide nicotinamide (niacinamide), where the carboxyl group has been replaced by a carboxamide group (CONH
2), as well as more complex amides and a variety of esters.[medical citation needed]
Niacin is available as a prescription product, and in the United States as a dietary supplement. Prescription products can be immediate release (Niacor, 500 mg tablets) or extended release (Niaspan, 500 and 1000 mg tablets). Dietary supplement products can be immediate or slow release, the latter including inositol hexanicotinate. The last has questionable clinical efficacy in reducing cholesterol levels.
Nicotinamide may be obtained from the diet where it is present primarily as NAD+ and NADP+. These are hydrolysed in the intestine and the resulting nicotinamide is absorbed either as such, or following its hydrolysis, to niacin. Nicotinamide may be toxic to the liver at doses exceeding 3 g/day for adults.
A prescription extended release niacin, Niaspan, has a film coating that delays release of the niacin, resulting in an absorption over a period of 8–12 hours. The extended release formulations generally reduce vasodilation and flushing side effects, but increase the risk of hepatotoxicity compared to the immediate release forms.
A combination of niacin and laropiprant had been approved for use in Europe and marketed as Tredaptive. Laropiprant is a prostaglandin D2 binding drug shown to reduce vasodilatation and flushing up to 73%. A clinical trial showed no additional efficacy of Tredaptive in lowering cholesterol when used together with other statin drugs, but did show an increase in other side effects. The study resulted in the withdrawal of Tredaptive from the international market.
One form of dietary supplement is inositol hexanicotinate (IHN), also called inositol nicotinate, which is inositol that has been esterified with niacin on all six of inositol's alcohol groups. IHN is usually sold as "flush-free" or "no-flush" niacin in units of 250, 500, or 1000 mg/tablets or capsules. In the US, it is sold as an over-the-counter formulation, and often is marketed and labeled as niacin, thus misleading consumers into thinking they are getting an active form of the medication. While this form of niacin does not cause the flushing associated with the immediate-release products, the evidence that it has lipid-modifying functions is disputed. As most of the clinical trials date from the early 1960s or the late 1970s, it is difficult to assess them by today's standards. Thus, so far there is not enough evidence to recommend IHN to treat dyslipidemia.
In 1942, when flour enrichment with nicotinic acid began, a headline in the popular press said "Tobacco in Your Bread." In response, the Council on Foods and Nutrition of the American Medical Association approved of the Food and Nutrition Board's new names niacin and niacin amide for use primarily by non-scientists. It was thought appropriate to choose a name to dissociate nicotinic acid from nicotine, to avoid the perception that vitamins or niacin-rich food contains nicotine, or that cigarettes contain vitamins. The resulting name niacin was derived from nicotinic acid + vitamin.
Niacin was first described by chemist Hugo Weidel in 1873 in his studies of nicotine. The original preparation remains useful: the oxidation of nicotine using nitric acid. For the first time, niacin was extracted by Casimir Funk, but he thought that it was thiamine and due to the discovered amine group he coined the term "vitamine". Niacin was extracted from livers by biochemist Conrad Elvehjem in 1937, who later identified the active ingredient, then referred to as the "pellagra-preventing factor" and the "anti-blacktongue factor." Soon after, in studies conducted in Alabama and Cincinnati, Dr. Tom Spies found that nicotinic acid cured the sufferers of pellagra.
Niacin is referred to as vitamin B3 because it was the third of the B vitamins to be discovered. It has historically been referred to as "vitamin PP", "vitamin P-P" and "PP-factor", that are derived from the term "pellagra-preventive factor". Carpenter found in 1951, that niacin in corn is biologically unavailable, and can be released only in very alkaline lime water of pH 11. In 1955, Altschul and colleagues described niacin as having a lipid-lowering property. As such, niacin is the oldest known lipid-lowering drug.
In animal models and in vitro, niacin produces marked anti-inflammatory effects in a variety of tissues – including the brain, gastrointestinal tract, skin, and vascular tissue – through the activation of hydroxycarboxylic acid receptor 2 (HCA2), also known as niacin receptor 1 (NIACR1). Niacin has been shown to attenuate neuroinflammation and may have efficacy in treating neuroimmune disorders. Unlike niacin, nicotinamide does not activate NIACR1; however, both niacin and nicotinamide activate the G protein-coupled estrogen receptor (GPER) in vitro.
In 2014, concurring with earlier work in 2001, by Arizona State University, researchers from Pennsylvania State University working with NASA found niacin, pyridine carboxylic acids and pyridine dicarboxylic acids inside meteorites.
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