Niacin

Niacin, also known as nicotinic acid, is an organic compound and a form of

Niacin
vitamin B3, an essential human nutrient. It has the formula C6H5NO2 and
belongs to the group of thepyridinecarboxylic acid.

Niacin is obtained in the diet from a variety of whole and processed foods, with
highest contents in fortified packaged foods, tuna, some vegetable and other
animal sources. Some countries require its addition to grains.[2] Medication and
supplemental niacin are primarily used to treat high blood cholesterol and Names
pellagra (niacin deficiency). Insufficient niacin in the diet can cause nausea, skin Pronunciation /ˈnaɪəsɪn/
and mouth lesions, anemia, headaches, and tiredness. The lack of niacin may
Preferred IUPAC name
also be observed in pandemic deficiency diseases, which are caused by a lack of
Pyridine-3-carboxylic acid[1]
five crucial vitamins (niacin, vitamin C, thiamin, vitamin D, and vitamin A) and
are usually found in areas of widespread poverty and malnutrition. Other names
Nicotinic acid (INN)
This colorless, water-soluble solid is a derivative of pyridine, with a carboxyl
Bionic
group (COOH) at the 3-position. Other forms of vitamin B3 include the
Vitamin B3
corresponding amide nicotinamide (niacinamide), where the carboxyl group has
been replaced by a carboxamide group (CONH2), as well as more complex Vitamin PP
amides and a variety ofesters. Identifiers

Niacin and nicotinamide are both precursors of the coenzymes nicotinamide

CAS Number 59-67-6
adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate 3D model Interactive image
(NADP) in vivo.[3] NAD converts to NADP by phosphorylation in the presence (JSmol)
of the enzyme NAD+ kinase. NADP and NAD are coenzymes for many 3DMet B00073
dehydrogenases, participating in many hydrogen transfer processes.[4] NAD is Beilstein 109591
important in catabolism of fat, carbohydrate, protein, and alcohol, as well as cell Reference
signaling and DNA repair, and NADP mostly in anabolism reactions such as ChEBI CHEBI:15940
fatty acid and cholesterol synthesis.[4] High energy requirements (brain) or high
ChEMBL ChEMBL573
turnover rate (gut, skin) organs are usually the most susceptible to their
deficiency.[5] ChemSpider 913

Niacin supplementation has not been found useful for decreasing the risk of DrugBank DB00627
cardiovascular disease in those already on a statin,[6] but appears to be effective ECHA InfoCard 100.000.401
in those not taking a statin.[7] Although niacin and nicotinamide are identical in
EC Number 200-441-0
their vitamin activity, nicotinamide does not have the same pharmacological
effects (lipid-modifying effects) as niacin. Nicotinamide does not reduce
Gmelin 3340
Reference
cholesterol or cause flushing.[8] As the precursor for NAD and NADP, niacin is
IUPHAR/BPS 1588
also involved in DNA repair.[9][10]
KEGG D00049
MeSH Niacin
Contents PubChem CID 938
Medical uses RTECS number QT0525000
Treatment of deficiency
Abnormal lipids UNII 2679MF687A
Contraindications InChI
 Adverse effects SMILES
Facial flushing
Gastrointestinal and hepatic Properties
Diabetes Chemical C6H5NO2
Other formula
Pregnancy Molar mass 123.111 g·mol−1
Deficiency Appearance White, translucent
Dietary recommendations crystals
Food sources
Density 1.473 g cm−3
Pharmacology
Pharmacodynamics Melting point 237 °C; 458 °F;
Pharmacokinetics 510 K
Biosynthesis Solubility in 18 g L−1
Physical and chemical properties water
Laboratory synthesis log P 0.219
Preparations Acidity (pKa) 2.0, 4.85
Nicotinamide
Extended release Isoelectric point 4.75
Inositol hexanicotinate Refractive index 1.4936
(nD)
Rename
History Dipole moment 0.1271305813 D
Research Thermochemistry
References Std enthalpy of −344.9 kJ mol−1
External links
formation
(ΔfHo298 )
Std enthalpy of −2.73083 MJ mol−1
Medical uses combustion
(ΔcHo298 )
Pharmacology
Treatment of deficiency ATC code C04AC01 (WHO)
Niacin and niacinamide are used for prevention and treatment ofpellagra.[11] C10AD02 (WHO)
License data EU EMA: by Nicotinic

Abnormal lipids acid

Niacin has sometimes been used in addition to other lipid-lowering Routes of Intramuscular, by
administration mouth
medications.[12] Systematic reviews found no effect of niacin on cardiovascular
disease or death, in spite of raising HDL cholesterol, and reported side effects Pharmacokinetics:
including an increased risk ofdiabetes.[6][13][14] Biological half- 20–45 min
life

Contraindications Hazards
EU classification
Niacin is contraindicated with active liver disease, persistent elevated serum (DSD) (outdated) Xi
transaminases, active peptic ulcer disease, or arterial bleeding.[15]
R-phrases R36/37/38
(outdated)
Adverse effects S-phrases S26, S36
The most common adverse effects of niacin at relatively low doses (50–500 mg) (outdated)
are flushing (e.g., warmth, redness, itching or tingling), headache, abdominal
NFPA 704
pain, diarrhea, dyspepsia, nausea, vomiting, rhinitis, pruritus and rash.[15][16] 1
These can be minimized by initiating therapy at low dosages, increasing dosage 1 0
 [15]
gradually, and avoiding administration on an empty stomach.
Flash point 193 °C (379 °F;
The acute adverse effects of high-dose niacin therapy (1–3 grams/day) – which is
466 K)
commonly used in the treatment of hyperlipidemias – further include
Autoignition 365 °C (689 °F;
hypotension, fatigue, glucose intolerance and insulin resistance, heartburn,
temperature 638 K)
blurred or impaired vision, and macular edema.[16] With long-term use, the
adverse effects of high-dose niacin therapy also include hepatic dysfunction Except where otherwise noted, data are
given for materials in their standard
(associated with fatigue, nausea, and anorexia), hepatitis, and acute liver
state (at 25 °C [77 °F], 100 kPa).
failure;[16] these hepatotoxic effects of niacin occur more often when extended-
verify (what is ?)
release dosage forms are used.[16] The long-term use of niacin at high doses
(2 grams/day) also significantly increases the risk of cerebral hemorrhage, Infobox references
ischemic stroke, gastrointestinal ulceration and bleeding, diabetes, dyspepsia,
and diarrhea.[16]

Facial flushing
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.[17] Reduction of flushing focuses on altering or
blocking the prostaglandin-mediated pathway.[18] Slow- or "sustained"-release forms of niacin have been developed to lessen these
side effects.[19][20]

Prostaglandin (PGD2) is the primary cause of the flushing reaction, with serotonin appearing to have a secondary role in this
reaction.[21] The effect is mediated by prostaglandin E2 and D2 due to GPR109A activation of epidermal Langerhans cells and
keratinocytes.[22][23] 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.[24][25] Flushing was often thought to
[21]
involve histamine, but histamine has been shown not to be involved in the reaction.

Gastrointestinal and hepatic

Hepatotoxicity is possibly related to metabolism via amidation resulting in NAD production.[26] The time-release form has a lower
.[27]
therapeutic index for lowering serum lipids relative to this form of toxicity

Diabetes
The high doses of niacin used to improve the lipid profile have been shown to elevate blood sugar by 5-10%, thereby worsening
existing diabetes mellitus.[28]

One review found that niacin therapy was associated with an increase in the risk of new-onset diabetes over 3.6 years from 4.9% to
5.5%.[29]

Other
Side effects of heart arrhythmias have also been reported.[28] Increased prothrombin time and decreased platelet count have been
[15]
reported; therefore, these should be monitored closely in patients who are also taking anticoagulants.

Particularly the time-release variety, at extremely high doses, can cause acute toxic reactions.[30] 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.[31]
Pregnancy
Niacin in doses used to lower cholesterol levels has been associated with birth defects in laboratory animals, with possible
consequences for infant development inpregnant women.[28]

Deficiency
Between 1906 and 1940 more than 3 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 the late
1930s, studies by Tom Spies, Marion Blankenhorn, and Clark Cooper established
that niacin cured pellagra in humans. The disease was greatly reduced as a result.

At present, niacin deficiency is sometimes seen in developed countries, and it is

usually apparent in conditions of poverty, malnutrition, and chronic alcoholism.[32]
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 orhominy are not at risk of niacin deficiency.

Mild niacin deficiency has been shown to slow metabolism, causing decreased
tolerance to cold. A man with pellagra, which is caused
by a chronic lack of vitamin B3 in the
Severe deficiency of niacin in the diet causes the disease pellagra, which is diet
characterized by diarrhea, dermatitis, and dementia, as well as Casal's necklace
lesions on the lower neck, hyperpigmentation, thickening of the skin, inflammation
of the mouth and tongue, digestive disturbances, amnesia, delirium, and eventually death, if left untreated.[33] Common psychiatric
symptoms of niacin deficiency include irritability, poor concentration, anxiety, fatigue, restlessness, apathy, and depression.[33]
Studies have indicated that, in patients with alcoholic pellagra, niacin deficiency may be an important factor influencing both the
onset and severity of this condition. Patients with alcoholism typically experience increased intestinal permeability, leading to
negative health outcomes.

Hartnup disease is a hereditary nutritional disorder resulting in niacin deficiency.[33] 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.[33] Niacin synthesis is also deficient in
carcinoid syndrome, because of metabolic diversion of itsprecursor tryptophan to form serotonin.

Dietary recommendations
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.[35] 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. For women (including those pregnant or
lactating), men and children the PRI is 1.6 mg niacin per megajoule (MJ) of energy consumed. 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.[38] The 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
[39]
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 Dietary recommendations

as 1 mg NE = 1 mg niacin or 60 mg of the
Australia and New Zealand
essential amino acid tryptophan. This is [show]
because the amino acid is utilized to synthesize
RDI for niacin (mg Upper level of
Age group
the vitamin.[35][38] NE/day) [34] intake [34]
Infants 0–6 months 2 mg/d preformed niacin*
For U.S. food and dietary supplement labeling ND
Infants 7–12 months 4 mg/d NE*
purposes the amount in a serving is expressed
1–3 6 10
as a percent of Daily Value (%DV). For niacin
4–8 8 15
labeling purposes 100% of the Daily Value
9–13 12 20
was 20 mg, but as of 27 May 2016 it was
14–18 – 30
revised to 16 mg to bring it into agreement
19+ – 35
with the RDA.[40] A table of the old and new
Females 14+ 14
adult Daily Values is provided at Reference –
Males 14+ 16
Daily Intake. The original deadline to be in
Pregnant females 14–50 18 –
compliance was 28 July 2018, but on 29
Pregnant females 14–18 – 30
September 2017 the FDA released a proposed
Pregnant females 19–50 – 35
rule that extended the deadline to 1 January
Lactating females 14–50 17 –
2020 for large companies and 1 January 2021
Lactating females 14–18 – 30
for small companies.[41]
Lactating females 19–50 – 35

* Adequate Intake for infants [35]

Food sources Canada

[show]
Niacin is found in a variety of whole and
processed foods, including fortified packaged RDA of niacin (mg Tolerable upper
Age group (years)
NE/d) [36] intake level [36]
foods, meat from various animal sources,
0–6 months 2 mg/d preformed niacin*
seafoods, and spices.[42] ND
7–12 months 4 mg/d NE*
1–3 6 10
Among whole food sources with the highest
4–8 8 15
niacin content per 100 grams:
9–13 12 20
Meats Females 14–18 14
30
Males 14–18 16
cooked skipjack tuna, 18.8 mg
Females 19+ 14
cooked light meat turkey, 11.8 mg 35
Males 19+ 16
cooked, lean ground pork, 11.1 mg
cooked venison, 10.8 mg Pregnant females <18 18 30

cooked, lean veal, 8.0 mg Pregnant females 18–50 18 35

Lactating females <18 17 30
Plant foods and spices
Lactating females 18–50 17 35
sesame seed flour, 12.5 mg
ground ginger, 9.6 mg
dried tarragon, 9.0 mg
dried, green sweet peppers, 7.4 mg
grilled portobello mushrooms, 6.2 mg
roasted sunflower seeds, 4.1 mg
dehydrated apricots, 3.6 mg
baked potato, 3.1 mg
Fortified breakfast cereals have among the
highest niacin contents (more than 20 mg per
100 grams).[42] Whole grain flours, such as
from wheat, rice, barley or corn, and pasta European Food Safety Authority
[show]
have niacin contents in a range of 3–10 mg per
Gender Adequate Intake (mg NE/MJ) [37]
100 grams.[42]
Females 1.3
Males 1.6
Pharmacology Tolerable upper limit of Tolerable upper limit of
Age (years) Nicotinic acid Nicotinamide
(mg/day) [37] (mg/day) [37]

Pharmacodynamics 1–3 2 150

4–6 3 220
The therapeutic effects of niacin are partly
7–10 4 350
mediated through the activation of G protein-
11–14 6 500
coupled receptors, including niacin receptor 1
15–17 8 700
(NIACR1) and niacin receptor 2 (NIACR2)
which are highly expressed in adipose tissue, United States
[show]
spleen, immune cells, and keratinocytes, but
not in other expected organs such as liver, RDA for niacin (mg Tolerable upper intake
Age group
NE/day) level [35]
kidney, heart or intestine.[43][44] NIACR1 and
Infants 0–6 months 2*
NIACR2 inhibit cyclic adenosine ND**
Infants 6–12 months 4*
monophosphate (cAMP) production and thus
1–3 6 10
fat breakdown in adipose tissue and free fatty
4–8 8 15
acids available for liver to produce
9–13 12 20
triglycerides and very-low-density lipoproteins
Females 14–18 14 30
(VLDL) and consequently low-density
Males 14–18 16 30
lipoprotein (LDL).[26][45] A decrease in free
Females 19+ 14 35
fatty acids also suppresses liver expression of
Males 19+ 16 35
apolipoprotein C3 and PPARg coactivator-1b,
Pregnant females 14–18 18 30
thus increasing VLDL turnover and reducing
Pregnant females 19–50 18 35
its production.[46]
Lactating females 14–18 17 30

The mechanism behind niacin increasing HDL Lactating females 19–50 17 35

is not totally understood, but seems to occur in * Adequate intake for infants, as an RDA has yet to be established
** Not possible to establish; source of intake should be formula and food only [35]
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.[47] Finally, it stimulates the ABCA1 transporter in monocytes and macrophages and upregulates
peroxisome proliferator-activated receptor gamma, resulting in reverse cholesterol transport.[48]

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).[47]
Despite the importance of other cardiovascular risk factors, high HDL was associated with fewer cardiovascular events independent
of LDL reduction.[49][50] Other effects include anti-thrombotic and vascular inflammation, improving endothelial function, and
plaque stability.[51] 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.[52] Niacin also appears to upregulate brain-derived neurotrophic factor and tropomyosin receptor kinase B (TrkB)
expression.[53]

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 cholesterol levels
are increased by niacin through direct and indirect pathways, such as by decreasing cholesterylester transfer protein activity and
[54]
triglyceride levels, while increasing HDL cholesterol levels.

Pharmacokinetics

Biosynthesis
The liver can synthesize niacin from the essential amino acid
tryptophan, requiring 60 mg of tryptophan to make 1 mg of niacin.
Riboflavin, vitamin B6 and iron are required for the process.[35]

Physical and chemical properties

Laboratory synthesis
Several thousand tons of niacin are manufactured each year, starting
from 3-methylpyridine.

Preparations
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.[55][56]
The last has questionable clinical efficacy in reducing cholesterol Niacin, serotonin (5-hydroxytryptamine), and
levels.[57] melatonin biosynthesis from tryptophan

Nicotinamide
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 nicotinic acid. Nicotinamide is
present in nature in only small amounts, however it is the main form of vitamin B3 in plasma. In unprepared foods, niacin is present
mainly in the form of the cellular pyridine nucleotides NAD and NADP. Enzymatic hydrolysis of the co-enzymes can occur during
the course of food preparation. Boiling releases most of the total niacin present in sweet corn as nicotinamide (up to 55 mg/kg).

[58]
Nicotinamide may be toxic to the liver at doses exceeding 3 g/day for adults.

Extended release
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.[59][60]

A formulation of laropiprant (Merck & Co., Inc.) and niacin had previously 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%.[47][61][62][63]
The HPS2-THRIVE study,[64] a study sponsored by Merck, 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 complete
withdrawal of Tredaptive from the international market.[65][66][67]

Inositol hexanicotinate
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.[68] IHN is usually sold as "flush-free" or "no-flush" niacin in units
of 250, 500, or 1000 mg/tablets or capsules. 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 the 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 the clinical trials
date from the early 1960s (Dorner, Welsh) or the late 1970s (Ziliotto, Kruse, Agusti),
it is difficult to assess them by today's standards.[69] One of the last of those studies
affirmed the superiority of inositol and xantinol esters of nicotinic acid for reducing Inositol hexanicotinate
serum free fatty acid,[70] but other studies conducted during the same period found
no benefit.[71] Studies explain that this is primarily because "flush-free" preparations
do not contain any free nicotinic acid. A more recent placebo-controlled trial was small (n=11/group), but results after three months
at 1500 mg/day showed no trend for improvements in total cholesterol, LDL-C, HDL-C or triglycerides.[72] Thus, so far there is not
enough evidence to recommend IHN to treatdyslipidemia.

Rename
In 1942, when flour enrichment with nicotinic acid began, a headline in the popular press said "Tobacco in Your Bread." So the
Council on Foods and Nutrition of the American Medical Associationapproved 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 it from nicotine, to
avoid the perception that vitamins or niacin-rich food contains nicotine, or that cigarettes contain vitamins.[73] The resulting name
niacin was derived from nicotinic acid + vitamin.[74][75]

History
Niacin was first described by chemist Hugo Weidel in 1873 in his studies of nicotine.[76] The original preparation remains useful: the
oxidation of nicotine using nitric acid.[77] 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."[78] Soon after, in studies conducted in Alabama and Cincinnati, Dr. Tom Spies found that nicotinic acid cured
the sufferers of pellagra.[79]

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".[74] Carpenter found in 1951
that niacin in corn is biologically unavailable, and can be released only in very alkaline lime water of pH 11.[80] In 1955, Altschul
.[81] As such, niacin is the oldest known lipid-lowering drug.
and colleagues described niacin as having a lipid-lowering property

Research
In animal models and in vitro, niacin produces marked anti-inflammatory effects in a variety of tissues – including the brain,
gastrointestinal tract, skin, andvascular tissue – through the activation of NIACR1.[82][83][84][85] Niacin has been shown to attenuate
neuroinflammation and may have efficacy in treating neuroimmune disorders such as multiple sclerosis and Parkinson's
disease.[82][85] Unlike niacin, nicotinamide does not activate NIACR1; however, both niacin and nicotinamide activate the G protein-
coupled estrogen receptor(GPER) in vitro.[86]

In 2014, concurring with earlier work in 2001 by Arizona State University, researchers from Pennsylvania State University working
meteorites.[87]
with NASA found niacin, pyridine carboxylic acids and pyridine dicarboxylic acids inside

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External links
Vitamin B3 MS Spectrum
Niacin bound to proteinsin the PDB
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