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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2017/07/28 14:33:23」(JST)

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Niacin, also known as nicotinic acid, is an organic compound with the formula C
6H
5NO
2 and, depending on the definition used, one of the 20 to 80 essential human nutrients. Together with nicotinamide it makes up the group known as vitamin B₃ complex.^[2]

Medication and supplemental niacin are primarily used to treat high blood cholesterol and pellagra (niacin deficiency). Insufficient niacin in the diet can cause nausea, skin and mouth lesions, anemia, headaches, and tiredness. The lack of niacin may also be observed in pandemic deficiency disease, which is caused by a lack of five crucial vitamins (niacin, vitamin C, thiamin, vitamin D, and vitamin A) and is usually found in areas of widespread poverty and malnutrition. Niacin is provided in the diet from a variety of whole and processed foods, with highest contents in fortified packaged foods and meat from various animal sources. Some countries require its addition to grains.^[3]

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 Other forms of vitamin B₃ include the corresponding amide nicotinamide ("niacinamide"), where the carboxyl group has been replaced by a carboxamide group (CONH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. Nicotinic acid and niacinamide are convertible to each other with steady world demand rising from 8,500 tonnes per year in the 1980s to 40,000 in recent years.^[4]

Niacin cannot be directly converted to nicotinamide, but both compounds are precursors of the coenzymes nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP) in vivo.^[5] 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.^[6] 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.^[6] High energy requirements (brain) or high turnover rate (gut, skin) organs are usually the most susceptible to their deficiency.^[7]

Niacin supplementation has not been found useful for decreasing the risk of cardiovascular disease in those already on a statin,^[8] but appears to be effective in those not taking a statin.^[9] Although niacin and nicotinamide are identical in their vitamin activity, nicotinamide does not have the same pharmacological effects (lipid modifying effects) as niacin. Nicotinamide does not reduce cholesterol or cause flushing.^[10] As the precursor for NAD and NADP, niacin is also involved in DNA repair.^[11]^[12]

1 Dietary reference intake
- 1.1 Food sources
2 Deficiency
3 Medical uses
- 3.1 Abnormal lipids
- 3.2 Treatment of deficiency
4 Contraindications
5 Side effects
- 5.1 Facial flushing
- 5.2 Gastrointestinal and hepatic
- 5.3 Metabolic
- 5.4 Other
- 5.5 In pregnancy
6 Pharmacology
- 6.1 Pharmacodynamics
- 6.2 Pharmacokinetics
  - 6.2.1 Biosynthesis
7 Physical and chemical properties
- 7.1 Laboratory synthesis
8 Preparations
- 8.1 Nicotinic acid
  - 8.1.1 Extended release
- 8.2 Inositol hexanicotinate
- 8.3 Nicotinamide
9 History
10 Research
11 References
12 External links

Dietary reference intake

The Food and Nutrition Board of the U.S. Institute of Medicine updated Estimated Average Requirements (EARs) and Recommended Dietary Allowances (RDAs) for niacin in 1998. The current EARs for niacin for women and men ages 14 and up are 11 mg/day and 12 mg/day, respectively; the RDAs are 14 and 16 mg/day, respectively. RDAs are higher than EARs so as to identify amounts that will cover people with higher than average requirements. RDA for pregnancy equals 18 mg/day. RDA for lactation equals 17 mg/day. For infants up to 12 months the Adequate Intake (AI) is 2–4 mg/day. and for children ages 1–13 years the RDA increases with age from 6 to 12 mg/day. As for safety, the Food and Nutrition Board also sets Tolerable Upper Intake Levels (known as ULs) for vitamins and minerals when evidence is sufficient. In the case of niacin the UL is set at 35 mg/day.^[13] The European Food Safety Authority states that different upper limits should be set for nicotinic acids and nicotinamide, both of which are known as niacin. For nicotinic acid, they recommend a UL at 10 mg/day, while for nicotinamide, the UL is recommended to 900 mg/day except during pregnancy and lactation.^[14] Safety issues are presented at length in the Side Effects section. Collectively the EARs, RDAs, AIs and ULs are referred to as Dietary Reference Intakes.

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 was 20 mg, but as of May 2016 it has been revised to 16 mg. A table of the pre-change adult Daily Values is provided at Reference Daily Intake. Food and supplement companies have until July 28, 2018, to comply with the change.

Food sources

Niacin is found in a variety of whole and processed foods, including fortified packaged foods, meat from various animal sources, seafoods, and spices.^[15]

Among whole food sources with the highest niacin content per 100 grams:

Meats

cooked skipjack tuna, 18.8 mg
cooked light meat turkey, 11.8 mg
cooked, lean ground pork, 11.1 mg
cooked venison, 10.8 mg
cooked, lean veal, 8.0 mg

Plant foods and spices

sesame seed flour, 12.5 mg
ground ginger, 9.6 mg
dried tarragon, 9.0 mg
dried, green sweet peppers, 7.4 mg
grilled portabella 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).^[15] Whole grain flours, such as from wheat, rice, barley or corn, and pasta have niacin contents in a range of 3–10 mg per 100 grams.^[15]

Deficiency

A man with pellagra, which is caused by a chronic lack of vitamin B₃ in the diet.

Between 1906 and 1940 more than 3 million Americans were affected by pellagra with more than 100,000 deaths. Dr. 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 Dr. 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.^[16] It also tends to occur in areas where people eat maize (corn) as a staple food, since it is the only grain low in digestible niacin. A cooking technique called nixtamalization increases the bioavailability of niacin during maize meal/flour production.

Mild niacin deficiency has been shown to slow metabolism, causing decreased tolerance to cold.

Severe deficiency of niacin in the diet causes the disease pellagra, which is 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.^[17] Common psychiatric symptoms of niacin deficiency include irritability, poor concentration, anxiety, fatigue, restlessness, apathy, and depression.^[17] 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.^[17] 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. 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.^[17] Niacin synthesis is also deficient in carcinoid syndrome, because of metabolic diversion of its precursor tryptophan to form serotonin.

Medical uses

Abnormal lipids

Niacin is sometimes used in addition to other lipid-lowering medication.^[18] Systematic reviews do not find that taking niacin affected either cardiovascular disease or risk of death in those already taking a statin, in spite of raising HDL cholesterol.^[8]^[19] Niacin alone appears to reduce the rate of cardiovascular events, but not the rate of coronary or cardiovascular deaths.^[20]^[21]

Treatment of deficiency

Niacin and niacinamide are used for prevention and treatment of pellagra.^[22]

Contraindications

Niacin is contraindicated with active liver disease, persistent elevated serum transaminases, active peptic ulcer disease, or arterial bleeding.^[23]

Side effects

The most common adverse effects are flushing (e.g., warmth, redness, itching or tingling), headache, pain, 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.^[23] High doses of niacin often temporarily reduce blood pressure as a result of acute vasodilation.^[24] In the longer term, high-dose niacin use may persistently lower blood pressure in individuals with hypertension, but more research is needed to determine the extent of this effect.^[24]

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.^[25] Reduction of flushing focuses on altering or blocking the prostaglandin mediated pathway.^[26] Slow- or "sustained"-release forms of niacin have been developed to lessen these side effects.^[27]^[28] One study showed the incidence of flushing was significantly lower with a sustained-release formulation,^[29] though doses above 2 g per day have been associated with liver damage, in particular, with slow-release formulations.^[30]

Prostaglandin (PGD₂) is the primary cause of the flushing reaction, with serotonin appearing to have a secondary role in this reaction.^[31] The effect is mediated by prostaglandin E2 and D2 due to GPR109A activation of epidermal Langerhans cells and keratinocytes.^[32]^[33] 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.^[34]^[35] Flushing was often thought to involve histamine, but histamine has been shown not to be involved in the reaction.^[31]

Gastrointestinal and hepatic

Gastrointestinal complaints, such as indigestion, nausea and liver failure, have also been reported. Hepatotoxicity is possibly related to metabolism via amidation resulting in NAD production.^[36] The time-release form has a lower therapeutic index for lowering serum lipids relative to this form of toxicity.^[37]

Metabolic

Although high doses of niacin may elevate blood sugar, thereby worsening diabetes mellitus,^[30] recent studies show the actual effect on blood sugar to be only 5–10%. Patients with diabetes who continued to take anti-diabetes drugs containing niacin did not experience major blood glucose changes. Thus, overall, niacin continues to be recommended as a drug for preventing cardiovascular disease in patients with diabetes.

Hyperuricemia is another side effect of taking high-dose niacin and may exacerbate gout.^[38]

Other

Side effects of heart arrhythmias have also been reported.^[30]^{[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.^[23]

Particularly the time-release variety, at extremely high doses, can cause acute toxic reactions.^[39] 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.^[40]

In pregnancy

Niacin in doses used to lower cholesterol levels has been associated with birth defects in laboratory animals, with possible consequences for infant development in pregnant women.^[30]

Pharmacology

Pharmacodynamics

Niacin's therapeutic effects 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.^[41]^[42] 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) or "bad" cholesterol.^[36]^[43] Decrease in free fatty acids also suppress hepatic expression of apolipoprotein C3 (APOC3) and PPARg coactivator-1b (PGC-1b) thus increase VLDL turn over and reduce its production.^[44] It also inhibits diacylglycerol acyltransferase-2 (important hepatic TG synthesis).

The mechanism behind increasing HDL is not totally understood but it seems to be done in various ways. Niacin increases apolipoprotein A1 levels due to anti catabolic effects resulting in higher reverse cholesterol transport. It also inhibits HDL hepatic uptake, down-regulating production of the cholesterol ester transfer protein (CETP) gene.^[45] Finally, it stimulates the ABCA1 transporter in monocytes and macrophages and up-regulates peroxisome proliferator-activated receptor γ results in reverse cholesterol transport.^[46]

It 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).^[45] Despite the importance of other cardiovascular risk factors, high HDL was associated with fewer cardiovascular events independent of LDL reduction.^[47]^[48] Other effects include anti-thrombotic and vascular inflammation, improving endothelial function, and plaque stability.^[49] Adipokines are the adipocytes’ produced mediators. Some adipokines such as tumor necrosis factor (TNF)-a, interleukins and chemokines, have pro-inflammatory effect and some others such as adiponectin have anti-inflammatory effect that regulates inflammatory process, decrease vascular progression and atherosclerosis.^[50]

Niacin also appears to upregulate brain-derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) expression.^[51]

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) It has the ability to bind to the receptor HCAR2 thereby decreasing lipolysis and FFA flux to the liver for triglyceride synthesis;[11] and (3) increased apoB catabolism. On the other hand, HDL cholesterol levels are increased by niacin through direct and indirect pathways. (4) Niacin decreases CETP mass and activity, and this synergistic effect with the decrease in triglyceride levels, can indirectly raise HDL cholesterol levels. The study has also been able to show direct effects on the beta chain of ATP synthase (5) and on production (6) and hepatic uptake (7) of apoA-I also increase HDL cholesterol levels. Thus by affecting the pathway reducing lipid levels help in reducing CVD.^[52]

Pharmacokinetics

Niacin, serotonin (5-hydroxytryptamine), and melatonin biosynthesis from tryptophan

Biosynthesis

The liver can synthesize niacin from the essential amino acid tryptophan, requiring 60 mg of tryptophan to make one mg of niacin.^[53] Riboflavin, vitamin B₆ and iron are required in some of the reactions involved in the conversion of tryptophan to NAD.

Physical and chemical properties

Laboratory synthesis

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

Preparations

Many preparations of niacin are available over-the-counter as dietary supplements. Non-prescription extended release niacin, such as Endur-acin, which uses a wax matrix to delay release is available as well.^[54]

Over-the counter plain niacin has FDA regulatory approval.^[55] Some “no flush” types, such as inositol hexanicotinate contain convertible niacin compounds, but have little clinical efficacy in reducing cholesterol levels.^[56]^[57] “Slow release” varieties have higher hepatotoxic activity, hence some types of prescription niacin are not recommended due to potential harm.^[58]

Nicotinic acid

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]

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%.^[45]^[60]^[61]^[62] The HPS2-THRIVE study,^[63] 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.^[64]^[65]^[66]

Inositol hexanicotinate

One form of dietary supplement is inositol hexanicotinate (IHN), which is inositol that has been esterified with niacin on all six of inositol's alcohol groups.^[67] 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.^[68] One of the last of those studies affirmed the superiority of inositol and xantinol esters of nicotinic acid for reducing serum free fatty acid,^[69] but other studies conducted during the same period found no benefit.^[70] 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.^[71] Thus, so far there is not enough evidence to recommend IHN to treat dyslipidemia.

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. 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).

Nicotinamide may be toxic to the liver at doses exceeding 3 g/day for adults.^[72]

History

Niacin was first described by chemist Hugo Weidel in 1873 in his studies of nicotine.^[73] The original preparation remains useful: the oxidation of nicotine using nitric acid.^[74] 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."^[75] Soon after, in studies conducted in Alabama and Cincinnati, Dr. Tom Spies found that nicotinic acid cured the sufferers of pellagra.^[76]

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".^[77] When the biological significance of nicotinic acid was realized, 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.^[78] The resulting name 'niacin' was derived from nicotinic acid + vitamin.^[77]^[79]

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 and colleagues described niacin as having a lipid lowering property.^[81] As such, niacin is the oldest lipid lowering drug.

Research

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 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]

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^ Maciejewski-Lenoir D, Richman JG, Hakak Y, Gaidarov I, Behan DP, Connolly DT (2006). "Langerhans cells release prostaglandin D2 in response to nicotinic acid". The Journal of Investigative Dermatology. 126 (12): 2637–46. PMID 17008871. doi:10.1038/sj.jid.5700586.
^ ^a ^b Gille A, Bodor ET, Ahmed K, Offermanns S (2008). "Nicotinic acid: Pharmacological effects and mechanisms of action". Annual Review of Pharmacology and Toxicology. 48 (1): 79–106. PMID 17705685. doi:10.1146/annurev.pharmtox.48.113006.094746.
^ Rader JI, Calvert RJ, Hathcock JN (January 1992). "Hepatic toxicity of unmodified and time-release preparations of niacin". The American Journal of Medicine. 92 (1): 77–81. PMID 1731514. doi:10.1016/0002-9343(92)90018-7.
^ Capuzzi DM, Morgan JM, Brusco OA, Intenzo CM (2000). "Niacin dosing: relationship to benefits and adverse effects". Curr Atheroscler Rep. 2 (1): 64–71. PMID 11122726. doi:10.1007/s11883-000-0096-y.
^ Mittal MK, Florin T, Perrone J, Delgado JH, Osterhoudt KC (2007). "Toxicity from the use of niacin to beat urine drug screening". Ann Emerg Med. 50 (5): 587–90. PMID 17418450. doi:10.1016/j.annemergmed.2007.01.014.
^ Gass JD (2003). "Nicotinic acid maculopathy". Retina (Philadelphia, Pa.). 23 (6 Suppl): 500–10. PMID 15035390.
^ Soga T, Kamohara M, Takasaki J, Matsumoto S, Saito T, Ohishi T, Hiyama H, Matsuo A, Matsushime H, Furuichi K (2003). "Molecular identification of nicotinic acid receptor". Biochemical and Biophysical Research Communications. 303 (1): 364–9. PMID 12646212. doi:10.1016/S0006-291X(03)00342-5.
^ Wise A, Foord SM, Fraser NJ, Barnes AA, Elshourbagy N, Eilert M, Ignar DM, Murdock PR, Steplewski K, Green A, Brown AJ, Dowell SJ, Szekeres PG, Hassall DG, Marshall FH, Wilson S, Pike NB (2003). "Molecular identification of high and low affinity receptors for nicotinic acid". The Journal of Biological Chemistry. 278 (11): 9869–74. PMID 12522134. doi:10.1074/jbc.M210695200.
^ Wanders D, Judd RL (2011). "Future of GPR109A agonists in the treatment of dyslipidaemia". Diabetes, obesity & metabolism. 13 (8): 685–91. PMID 21418500. doi:10.1111/j.1463-1326.2011.01400.x.
^ Hernandez C, Molusky M, Li Y, Li S, Lin JD (2010). "Regulation of hepatic ApoC3 expression by PGC-1β mediates hypolipidemic effect of nicotinic acid". Cell Metabolism. 12 (4): 411–9. PMC 2950832 . PMID 20889132. doi:10.1016/j.cmet.2010.09.001.
^ ^a ^b ^c Villines TC, Kim AS, Gore RS, Taylor AJ (2012). "Niacin: The evidence, clinical use, and future directions". Current atherosclerosis reports. 14 (1): 49–59. PMID 22037771. doi:10.1007/s11883-011-0212-1.
^ Rubic T, Trottmann M, Lorenz RL (2004). "Stimulation of CD36 and the key effector of reverse cholesterol transport ATP-binding cassette A1 in monocytoid cells by niacin". Biochemical Pharmacology. 67 (3): 411–9. PMID 15037193. doi:10.1016/j.bcp.2003.09.014.
^ Barter P, Gotto AM, LaRosa JC, Maroni J, Szarek M, Grundy SM, Kastelein JJ, Bittner V, Fruchart JC (2007). "HDL cholesterol, very low levels of LDL cholesterol, and cardiovascular events". The New England Journal of Medicine. 357 (13): 1301–10. PMID 17898099. doi:10.1056/NEJMoa064278.
^ Jafri H, Alsheikh-Ali AA, Karas RH (2010). "Meta-analysis: Statin therapy does not alter the association between low levels of high-density lipoprotein cholesterol and increased cardiovascular risk". Annals of Internal Medicine. 153 (12): 800–8. PMID 21173414. doi:10.7326/0003-4819-153-12-201012210-00006.
^ Wu BJ, Yan L, Charlton F, Witting P, Barter PJ, Rye KA (2010). "Evidence that niacin inhibits acute vascular inflammation and improves endothelial dysfunction independent of changes in plasma lipids". Arteriosclerosis, thrombosis, and vascular biology. 30 (5): 968–75. PMID 20167660. doi:10.1161/ATVBAHA.109.201129.
^ Gustafson B (2010). "Adipose tissue, inflammation and atherosclerosis". Journal of atherosclerosis and thrombosis. 17 (4): 332–41. PMID 20124732. doi:10.5551/jat.3939.
^ Fu L, Doreswamy V, Prakash R (2014). "The biochemical pathways of central nervous system neural degeneration in niacin deficiency". Neural Regen Res. 9 (16): 1509–1513. PMC 4192966 . PMID 25317166. doi:10.4103/1673-5374.139475. Recent evidences suggest that niacin administration may up-regulate the expression of BDNF-TrkB. ... At present, we can safely raise the possibility that niacin-mediated neural growth by the BDNF-TrkB pathway could be at least partially mediated by enhanced HDL-C levels.
^ Creider, JC; Hegele, RA; Joy, TR (September 2012). "Niacin: another look at an underutilized lipid-lowering medication.". Nature Reviews. Endocrinology. 8 (9): 517–28. PMID 22349076. doi:10.1038/nrendo.2012.22.
^ Jacobson, EL (2007). "Niacin". Linus Pauling Institute. Retrieved 31 March 2008.
^ Dunatchik, Andrew P.; Ito, Matthew K.; Dujovne, Carlos A. (2012-03-01). "A systematic review on evidence of the effectiveness and safety of a wax-matrix niacin formulation". Journal of Clinical Lipidology. 6 (2): 121–131. ISSN 1933-2874. PMID 22385545. doi:10.1016/j.jacl.2011.07.003.
^ Meyers, C. Daniel; Carr, Molly C.; Park, Sang; Brunzell, John D. (2003-12-16). "Varying cost and free nicotinic acid content in over-the-counter niacin preparations for dyslipidemia". Annals of Internal Medicine. 139 (12): 996–1002. ISSN 1539-3704. PMID 14678919. doi:10.7326/0003-4819-139-12-200312160-00009.
^ Keenan, Joseph M. (2013-01-01). "Wax-matrix extended-release niacin vs inositol hexanicotinate: a comparison of wax-matrix, extended-release niacin to inositol hexanicotinate "no-flush" niacin in persons with mild to moderate dyslipidemia". Journal of Clinical Lipidology. 7 (1): 14–23. ISSN 1933-2874. PMID 23351578. doi:10.1016/j.jacl.2012.10.004.
^ Norris RB (2006). ""Flush-free niacin": Dietary supplement may be "benefit-free"". Preventive cardiology. 9 (1): 64–5. PMID 16407706. doi:10.1111/j.1520-037X.2006.04736.x.
^ Bassan M (2012). "A case for immediate-release niacin". Heart Lung. 41: 95–8. PMID 21414665. doi:10.1016/j.hrtlng.2010.07.019.
^ Reiche, Ines; Westphal, Sabine; Martens-Lobenhoffer, Jens; Tröger, Uwe; Luley, Claus; Bode-Böger, Stefanie M. (2011-01-01). "Pharmacokinetics and dose recommendations of Niaspan® in chronic kidney disease and dialysis patients". Nephrology, Dialysis, Transplantation: Official Publication of the European Dialysis and Transplant Association - European Renal Association. 26 (1): 276–282. ISSN 1460-2385. PMID 20562093. doi:10.1093/ndt/gfq344.
^ Lai E, De Lepeleire I, Crumley TM, Liu F, Wenning LA, Michiels N, Vets E, O'Neill G, Wagner JA, Gottesdiener K (2007). "Suppression of niacin-induced vasodilation with an antagonist to prostaglandin D2 receptor subtype 1". Clinical pharmacology and therapeutics. 81 (6): 849–57. PMID 17392721. doi:10.1038/sj.clpt.6100180.
^ Paolini JF, Bays HE, Ballantyne CM, Davidson M, Pasternak R, Maccubbin D, Norquist JM, Lai E, Waters MG, Kuznetsova O, Sisk CM, Mitchel YB (November 2008). "Extended-release niacin/laropiprant: reducing niacin-induced flushing to better realize the benefit of niacin in improving cardiovascular risk factors". Cardiol Clin. 26 (4): 547–60. PMID 19031552. doi:10.1016/j.ccl.2008.06.007.
^ Kamanna VS, Vo A, Kashyap ML (2008). "Nicotinic acid: Recent developments". Current Opinion in Cardiology. 23 (4): 393–8. PMID 18520725. doi:10.1097/HCO.0b013e3283021c82. .
^ "Treatment of HDL to Reduce the Incidence of Vascular Events HPS2-THRIVE - Full Text View - ClinicalTrials.gov". clinicaltrials.gov. Retrieved 2017-02-20.
^ Medscape: Medscape Access
^ Nainggolan, Lisa (2013-01-11). "Niacin/Laropiprant Products to Be Suspended Worldwide". Medscape. Retrieved 2017-02-20.
^ "Merck begins overseas recall of HDL cholesterol drug". Reuters. 11 January 2013.
^ F. Aguilar; U.R. Charrondiere; B. Dusemund; P. Galtier; J. Gilbert; D.M. Gott; S. Grilli; R. Guertler; G.E.N. Kass; J. Koenig; C. Lambré; J-C. Larsen; J-C. Leblanc; A. Mortensen; D. Parent-Massin; I. Pratt; I.M.C.M. Rietjens; I. Stankovic; P. Tobback; T. Verguieva; R.A. Woutersen (2009). "Inositol hexanicotinate (inositol hexaniacinate) as a source of niacin (vitamin B3) added for nutritional purposes in food supplements". The EFSA Journal. 949: 1–20.
^ Taheri, R (15 January 2003). "No-Flush Niacin for the Treatment of Hyperlipidemia". Medscape. Retrieved 31 March 2008.
^ Kruse W, Kruse W, Raetzer H, Heuck CC, Oster P, Schellenberg B, Schlierf G (1979). "Nocturnal inhibition of lipolysis in man by nicotinic acid and derivatives". European Journal of Clinical Pharmacology. 16 (1): 11–15. PMID 499296. doi:10.1007/BF00644960.
^ Meyers CD, Carr MC, Park S, Brunzell JD (2003). "Varying cost and free nicotinic acid content in over-the-counter niacin preparations for dyslipidemia" (PDF). Annals of Internal Medicine. 139 (12): 996–1002. PMID 14678919. doi:10.7326/0003-4819-139-12-200312160-00009.
^ Benjó AM, Maranhão RC, Coimbra SR, Andrade AC, Favarato D, Molina MS, Brandizzi LI, da Luz PL (2006). "Accumulation of chylomicron remnants and impaired vascular reactivity occur in subjects with isolated low HDL cholesterol: effects of niacin treatment". Atherosclerosis. 187 (1): 116–122. PMID 16458316. doi:10.1016/j.atherosclerosis.2005.08.025.
^ Knip M, Douek IF, Moore WP, Gillmor HA, McLean AE, Bingley PJ, Gale EA (2000). "Safety of high-dose nicotinamide: a review". Diabetologia. 43 (11): 1337–45. PMID 11126400. doi:10.1007/s001250051536.
^ Weidel, H (1873). "Zur Kenntniss des Nicotins". Justus Liebigs Annalen der Chemie und Pharmacie. 165 (2): 330–349. doi:10.1002/jlac.18731650212.
^ Samuel M. McElvain (1941). "Nicotinic Acid" (PDF). Org. Synth. ; Coll. Vol., 1, p. 385
^ Elvehjem CA, Madden RJ, Strongandd FM, Woolley DW (1938). "The isolation and identification of the anti-blacktongue factor J" (PDF). J. Biol. Chem. 123 (1): 137–149.
^ Kraut, Alan. "Dr. Joseph Goldberger and the War on Pellagra | Ashes on the Potomac". history.nih.gov. Retrieved 2017-02-20.
^ ^a ^b "Pellagra And Its Prevention And Control In Major Emergencies" (PDF). World Health Organization. World Health Organization. Retrieved 17 April 2015.
^ "Niacin and Nicotinic Acid". Journal of the American Medical Association. American Medical Association. 118 (10): 823. March 7, 1942. doi:10.1001/jama.1942.02830100053014. Retrieved May 7, 2016.
^ "Niacin and Niacin Amide". Journal of the American Medical Association. American Medical Association. 118 (10): 819. March 7, 1942. doi:10.1001/jama.1942.02830100049011. Retrieved May 7, 2016.
^ Laguna J, Carpenter KJ (September 1951). "Raw versus processed corn in niacin-deficient diets". J. Nutr. 45 (1): 21–8. PMID 14880960.
^ Altschul R, Hoffer A, Stephen JD (1955). "Influence of nicotinic acid on serum cholesterol in man". Archives of Biochemistry and Biophysics. 54 (2): 558–9. PMID 14350806. doi:10.1016/0003-9861(55)90070-9.
^ ^a ^b Offermanns S, Schwaninger M (2015). "Nutritional or pharmacological activation of HCA(2) ameliorates neuroinflammation". Trends Mol Med. 21 (4): 245–255. PMID 25766751. doi:10.1016/j.molmed.2015.02.002. Neuroinflammatory cells express HCA2, a receptor for the endogenous neuroprotective ketone body β-hydroxybutyrate (BHB) as well as for the drugs dimethyl fumarate (DMF) and nicotinic acid, which have established efficacy in the treatment of MS and experimental stroke, respectively. This review summarizes the evidence that HCA2 is involved in the therapeutic effects of DMF, nicotinic acid, and ketone bodies in reducing neuroinflammation.
^ Chai JT, Digby JE, Choudhury RP (May 2013). "GPR109A and vascular inflammation". Curr Atheroscler Rep. 15 (5): 325. PMC 3631117 . PMID 23526298. doi:10.1007/s11883-013-0325-9. As GPR109A's primary pharmacological ligand in clinical use, niacin has been used for over 50 years in the treatment of cardiovascular disease, mainly due to its favourable effects on plasma lipoproteins.
^ Graff EC, Fang H, Wanders D, Judd RL (February 2016). "Anti-inflammatory effects of the hydroxycarboxylic acid receptor 2". Metab. Clin. Exp. 65 (2): 102–113. PMID 26773933. doi:10.1016/j.metabol.2015.10.001. HCA2 is highly expressed on immune cells, including macrophages, monocytes, neutrophils and dermal dendritic cells, among other cell types. ... Recent studies demonstrate that HCA2 mediates profound anti-inflammatory effects in a variety of tissues.
^ ^a ^b Wakade C, Chong R (December 2014). "A novel treatment target for Parkinson's disease". J. Neurol. Sci. 347 (1–2): 34–38. PMID 25455298. doi:10.1016/j.jns.2014.10.024.
^ Santolla MF, De Francesco EM, Lappano R, Rosano C, Abonante S, Maggiolini M (July 2014). "Niacin activates the G protein estrogen receptor (GPER)-mediated signalling". Cell. Signal. 26 (7): 1466–1475. PMID 24662263. doi:10.1016/j.cellsig.2014.03.011. Nicotinic acid, also known as niacin, is the water soluble vitamin B3 used for decades for the treatment of dyslipidemic diseases. Its action is mainly mediated by the G protein-coupled receptor (GPR) 109A.

External links

Vitamin B3 MS Spectrum
Niacin bound to proteins in the PDB

UpToDate Contents

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1. スタチン系およびフィブラート系以外の薬剤による脂質低下 lipid lowering with drugs other than statins and fibrates
2. 水溶性ビタミンの概要 overview of water soluble vitamins
3. 成人の顔面紅潮に対するアプローチ approach to flushing in adults
4. 高トリグリセリド血症患者に対するアプローチ approach to the patient with hypertriglyceridemia
5. 心血管疾患または糖尿病患者におけるコレステロール低下に関する臨床試験 clinical trials of cholesterol lowering in patients with cardiovascular disease or diabetes

English Journal

A comparative study of ICH validated novel spectrophotometric techniques for resolving completely overlapping spectra of quaternary mixtures.

Ali NW1, Abdelwahab NS2, Abdelkawy M3, Emam AA2.
Spectrochimica acta. Part A, Molecular and biomolecular spectroscopy.Spectrochim Acta A Mol Biomol Spectrosc.2016 Feb 5;154:114-22. doi: 10.1016/j.saa.2015.10.037. Epub 2015 Oct 24.
A pharmaceutically marketed mixture of Yohimbine, Alpha-tocopheryl acetate, Niacin, and Caffeine co-formulated as a promising therapy for erectile dysfunction. Simultaneous determination of the aforementioned pharmaceutical formulation without prior separation steps was applied using mean centering
PMID 26519919

A Nampt inhibitor FK866 mimics vitamin B3 deficiency by causing senescence of human fibroblastic Hs68 cells via attenuation of NAD(+)-SIRT1 signaling.

Song TY1, Yeh SL2,3, Hu ML4, Chen MY2, Yang NC5,6.
Biogerontology.Biogerontology.2015 Dec;16(6):789-800. doi: 10.1007/s10522-015-9605-9. Epub 2015 Sep 2.
Vitamin B3 (niacin) deficiency can cause pellagra with symptoms of dermatitis, diarrhea and dementia. However, it is unclear whether the vitamin B3 deficiency causes human aging. FK866 (a Nampt inhibitor) can reduce intracellular NAD(+) level and induce senescence of human Hs68 cells. However, the m
PMID 26330291

Niacin as antidyslipidemic drug.

Julius U1,2.
Canadian journal of physiology and pharmacology.Can J Physiol Pharmacol.2015 Dec;93(12):1043-54. doi: 10.1139/cjpp-2014-0478. Epub 2015 Apr 28.
Niacin is an important vitamin (B3) that can be used in gram doses to positively modify pathogenetically relevant lipid disorders: elevated LDL cholesterol, elevated non-HDL cholesterol, elevated triglycerides, elevated lipoprotein(a), and reduced HDL cholesterol. This review reports the latest publ
PMID 26370906

Japanese Journal

Niacin ameliorates ulcerative colitis via prostaglandin D2‐mediated D prostanoid receptor 1 activation

EMBO molecular medicine 9(5), 571-588, 2017-05
NAID 120006224674

食品中ビタミンの調理損耗に関するレビュー(その2)ナイアシン,パントテン酸,ビオチン,葉酸,ビタミンC

ビタミン = Vitamins 91(2), 87-112, 2017-02
NAID 40021110074

一般向けビタミン主薬製剤及びビタミン含有保健薬の水溶性ビタミン配合量に基づく類似性分析

薬学雑誌 137(5), 595-602, 2017
NAID 130005631390

Related Pictures

★リンクテーブル★

リンク元	「ナイアシン」「ピルビン酸デヒドロゲナーゼ」「ニコチン酸」「pertain」「ビタミンB」
拡張検索	「niacinamide」「xanthinol niacinate」

「ナイアシン」

Niacin
Names
	Preferred IUPAC name Pyridine-3-carboxylic acid
	Other names Nicotinic acid (INN); Bionic; Vitamin B3; Vitamin PP
Identifiers
CAS Number	59-67-6 ;
3D model (JSmol)	Interactive image;
3DMet	B00073
Beilstein Reference	109591
ChEBI	CHEBI:15940 ;
ChemSpider	913 ;
DrugBank	DB00627 ;
ECHA InfoCard	100.000.401
EC Number	200-441-0
Gmelin Reference	3340
IUPHAR/BPS	1588;
KEGG	D00049 ;
MeSH	Niacin
PubChem CID	938;
RTECS number	QT0525000
UNII	2679MF687A ;
	InChI InChI=1S/C6H5NO2/c8-6(9)5-2-1-3-7-4-5/h1-4H,(H,8,9) Key: PVNIIMVLHYAWGP-UHFFFAOYSA-N ; InChI=1/C6H5NO2/c8-6(9)5-2-1-3-7-4-5/h1-4H,(H,8,9) Key: PVNIIMVLHYAWGP-UHFFFAOYAA ;
	SMILES OC(=O)c1cccnc1 ;
Properties
Chemical formula	C; 6NH; 5O; 2
Molar mass	123.1094 g mol−1
Appearance	White, translucent crystals
Density	1.473 g cm−3
Melting point	237 °C; 458 °F; 510 K
Solubility in water	18 g L−1
log P	0.219
Acidity (pKa)	2.0,4.85
Isoelectric point	4.75
Refractive index (nD)	1.4936
Dipole moment	0.1271305813 D
Thermochemistry
Std enthalpy of; formation (ΔfHo298)	−344.9 kJ mol−1
Std enthalpy of; combustion (ΔcHo298)	−2.73083 MJ mol−1
Pharmacology
ATC code	C04AC01 (WHO) C10AD02 (WHO)
Routes of; administration	Intramuscular, Oral
	Pharmacokinetics:
Biological half-life	20–45 min
Hazards
EU classification (DSD) (outdated)	Xi
R-phrases (outdated)	R36/37/38
S-phrases (outdated)	S26, S36
NFPA 704	1 1 0
Flash point	193 °C (379 °F; 466 K)
Autoignition; temperature	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).
	verify (what is ?)
	Infobox references

　　[★]

英: niacin
同: ビタミンB3？
関: nicotinamide, ニコチン酸 nicotinic acid nicotinic acid、ビタミン; Nicobid？

ビタミンB複合体の一つ。ニコチン酸とニコチン酸アミドがある。
ナイアシンはニコチン酸、ニコチンアミド、および生体内で活性を持つこれらの誘導体を総称していう(HIM.442)

⇔FB.196ではナイアシン = ニコチン酸、ナイアシンアミド = ニコチン酸アミドとしている。

厳密に言えば、生体内でトロプトファンから合成できる(その際にビタミンB6とriboflavinが必要)ので、ビタミンではない。トリプトファン60mgでナイアシン1mgに換算できる。ナイアシンはNADとなって、生体内で、酸化還元酵素の補酵素として機能するが、その他に、蛋白のADPリボシル化におけるADPリボースの供給源として、またDNA修復機構に関与するnucleoproteinのポリADPリボシル化にも関与している。(HBC.498)

臨床関連

ペラグラ：ナイアシン欠乏症
過剰摂取：(1-6g/dayのナイアシン服用は高脂血症治療のために用いられる)血管拡張・紅潮、皮膚の刺激感。(500mg/day以上の摂取)肝障害。(HBC.498)

「ピルビン酸デヒドロゲナーゼ」

　　[★]

英: pyruvate dehydrogenase
関: ピルビン酸脱水素酵素、ピルビン酸、ピルビン酸デヒドロゲナーゼ複合体

概要

ピルビン酸からアセチルCoAを生成し、クエン酸回路に投入するための酵素
逆反応を触媒する酵素はない

反応

ピルビン酸+NAD⁺+SH-CoA　→　アセチルCoA+NADH+CO₂

補酵素

臨床関連

不足

ピルビン酸脱水素酵素欠損症

ピルビン酸、アラニンの蓄積→乳酸アシドーシス

アルコール中毒によるビタミンB1不足によっても生じる

「ニコチン酸」

　　[★]

英: nicotinic acid nicotinate NiA
同: ナイアシン niacin、ビタミンB3、3-ピリジンカルボン酸 3-pyridinecarboxylic acid
商: ナイクリン
関: NAD、ペラグラ、ビタミン

概念

ビタミンの一つ。

ビタミンB複合体の一つで、ビタミンB3。別名、ナイアシン(和文ではニコチン酸、英文ではナイアシンという記載をよく見かける、気がする)

トリプトファンからも合成される。
高脂血症薬としても使われる

臨床関連

ナイアシン欠乏症

ペラグラを来す

参考

構造

http://fptsukioka555.blog86.fc2.com/blog-entry-14.html

wiki ja

http://ja.wikipedia.org/wiki/%E3%83%8B%E3%82%B3%E3%83%81%E3%83%B3%E9%85%B8

wiki en

http://en.wikipedia.org/wiki/%E3%83%8B%E3%82%B3%E3%83%81%E3%83%B3%E9%85%B8

「pertain」

　　[★]

vi.

付属する、属する(to)。適する、似合う(to)。関係する(to)

However, this upper limit does not pertain to the therapeutic use of niacin.(HIM.444)(この上限はナイアシンの治療目的の使用には関係ない)

Information on key trial characteristics, including information pertaining to the risk of bias were extracted and recorded.

関: belong, concern, connect, connection, correlation, germane, implicate, interplay, pertinent, referable, relate, relation, relationship, reside, respect

「ビタミンB」

　　[★]

英: vitamin B
関: ビタミン; thiamine、niacin、pyridoxine

「niacinamide」

　　[★] ナイアシンアミド

関: ニコチン酸アミド nicotinamide、vitamin B3

ビタミンB群の補酵素

「xanthinol niacinate」

　　[★]

ニコチン酸キサンチノール

関: xantinol nicotinate

[iupac2013-1] Nomenclature of Organic Chemistry : IUPAC Recommendations and Preferred Names 2013 (Blue Book). Cambridge: The Royal Society of Chemistry. 2014. pp. 747, 750. ISBN 978-0-85404-182-4. doi:10.1039/9781849733069-FP001.

[2] Krutmann, Jean; Humbert, Philippe (2010). Nutrition for Healthy Skin: Strategies for Clinical and Cosmetic Practice. Springer Science & Business Media. p. 153. ISBN 9783642122644.

[3] "Why fortify?". Food Fortification Initiative. 2017. Retrieved 4 April 2017.

[4] Cantarella L, Gallifuoco A, Malandra A, Martínková L, Spera A, Cantarella M (2011). "High-yield continuous production of nicotinic acid via nitrile hydratase-amidase cascade reactions using cascade CSMRs". Enzyme and Microbial Technology. 48 (4–5): 345–50. PMID 22112948. doi:10.1016/j.enzmictec.2010.12.010.

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v t e Peripheral vasodilators (C04)
Phenylethanolamine derivatives	Isoxsuprine Buphenine Bamethan
Alpha blockers	Non-selective Tolazoline Phentolamine Selective α₁-blockers Alfuzosin Doxazosin Prazosin Silodosin Tamsulosin Terazosin
Niacin and derivatives	Niacin Nicotinyl alcohol Inositol nicotinate Ciclonicate
Purine derivatives	Pentifylline Xantinol nicotinate Pentoxifylline Etofylline nicotinate
Ergot alkaloids	Ergoloid Nicergoline Dihydroergocristine
Other peripheral vasodilators	Cyclandelate Phenoxybenzamine Vincamine Moxisylyte Bencyclane Vinburnine Sulcotidil Buflomedil Naftidrofuryl Butalamine Visnadine Cetiedil Cinepazide Ifenprodil Azapetine Fasudil

v t e GABA_A receptor PAMs
Alcohols	Brometone Butanol Chloralodol Chlorobutanol (cloretone) Ethanol (drinking alcohol) Ethchlorvynol Isobutanol Isopropanol Menthol Methanol Methylpentynol Pentanol Petrichloral Propanol tert-Butanol (2M2P) tert-Pentanol (2M2B) Tribromoethanol Trichloroethanol Triclofos Trifluoroethanol
Barbiturates	(-)-DMBB Allobarbital Alphenal Amobarbital Aprobarbital Barbexaclone Barbital Benzobarbital Benzylbutylbarbiturate Brallobarbital Brophebarbital Butabarbital/Secbutabarbital Butalbital Buthalital Butobarbital Butallylonal Carbubarb Crotylbarbital Cyclobarbital Cyclopentobarbital Difebarbamate Enallylpropymal Ethallobarbital Eterobarb Febarbamate Heptabarb Heptobarbital Hexethal Hexobarbital Metharbital Methitural Methohexital Methylphenobarbital Narcobarbital Nealbarbital Pentobarbital Phenallymal Phenobarbital Phetharbital Primidone Probarbital Propallylonal Propylbarbital Proxibarbital Reposal Secobarbital Sigmodal Spirobarbital Talbutal Tetrabamate Tetrabarbital Thialbarbital Thiamylal Thiobarbital Thiobutabarbital Thiopental Thiotetrabarbital Valofane Vinbarbital Vinylbital
Benzodiazepines	2-Oxoquazepam 3-Hydroxyphenazepam Adinazolam Alprazolam Arfendazam Avizafone Bentazepam Bretazenil Bromazepam Brotizolam Camazepam Carburazepam Chlordiazepoxide Ciclotizolam Cinazepam Cinolazepam Clazolam Climazolam Clobazam Clonazepam Clonazolam Clorazepate Clotiazepam Cloxazolam CP-1414S Cyprazepam Delorazepam Demoxepam Diazepam Diclazepam Doxefazepam Elfazepam Estazolam Ethyl carfluzepate Ethyl dirazepate Ethyl loflazepate Etizolam EVT-201 FG-8205 Fletazepam Flubromazepam Flubromazolam Fludiazepam Flunitrazepam Flurazepam Flutazolam Flutemazepam Flutoprazepam Fosazepam Gidazepam Halazepam Haloxazolam Iclazepam Imidazenil Irazepine Ketazolam Lofendazam Lopirazepam Loprazolam Lorazepam Lormetazepam Meclonazepam Medazepam Menitrazepam Metaclazepam Mexazolam Midazolam Motrazepam N-Desalkylflurazepam Nifoxipam Nimetazepam Nitrazepam Nitrazepate Nitrazolam Nordazepam Nortetrazepam Oxazepam Oxazolam Phenazepam Pinazepam Pivoxazepam Prazepam Premazepam Proflazepam Pyrazolam QH-II-66 Quazepam Reclazepam Remimazolam Rilmazafone Ripazepam Ro48-6791 Ro48-8684 SH-053-R-CH3-2′F Sulazepam Temazepam Tetrazepam Tolufazepam Triazolam Triflubazam Triflunordazepam (Ro5-2904) Tuclazepam Uldazepam Zapizolam Zolazepam Zomebazam
Carbamates	Carisbamate Carisoprodol Clocental Cyclarbamate Difebarbamate Emylcamate Ethinamate Febarbamate Felbamate Hexapropymate Lorbamate Mebutamate Meprobamate Nisobamate Pentabamate Phenprobamate Procymate Styramate Tetrabamate Tybamate
Flavonoids	6-Methylapigenin Ampelopsin (dihydromyricetin) Apigenin Baicalein Baicalin Catechin EGC EGCG Hispidulin Linarin Luteolin Rc-OMe Skullcap constituents (e.g., baicalin) Wogonin
Imidazoles	Etomidate Metomidate Propoxate
Kava constituents	10-Methoxyyangonin 11-Methoxyyangonin 11-Hydroxyyangonin Desmethoxyyangonin 11-Methoxy-12-hydroxydehydrokavain 7,8-Dihydroyangonin Kavain 5-Hydroxykavain 5,6-Dihydroyangonin 7,8-Dihydrokavain 5,6,7,8-Tetrahydroyangonin 5,6-Dehydromethysticin Methysticin 7,8-Dihydromethysticin Yangonin
Monoureides	Acecarbromal Apronal (apronalide) Bromisoval Carbromal Capuride Ectylurea
Neuroactive steroids	Acebrochol Allopregnanolone (brexanolone) Alfadolone Alfaxalone 3α-Androstanediol Androstenol Androsterone Certain anabolic-androgenic steroids Cholesterol DHDOC 3α-DHP 5α-DHP 5β-DHP DHT Etiocholanolone Ganaxolone Hydroxydione Minaxolone Org 20599 Org 21465 P1-185 Pregnanolone (eltanolone) Progesterone Renanolone SAGE-105 SAGE-217 SAGE-324 SAGE-516 SAGE-689 SAGE-872 Testosterone THDOC
Nonbenzodiazepines	β-Carbolines: Abecarnil Gedocarnil Harmane SL-651,498 ZK-93423; Cyclopyrrolones: Eszopiclone Pagoclone Pazinaclone Suproclone Suriclone Zopiclone; Imidazopyridines: Alpidem DS-1 Necopidem Saripidem Zolpidem; Pyrazolopyrimidines: Divaplon Fasiplon Indiplon Lorediplon Ocinaplon Panadiplon Taniplon Zaleplon; Others: Adipiplon CGS-8216 CGS-9896 CGS-13767 CGS-20625 CL-218,872 CP-615,003 CTP-354 ELB-139 GBLD-345 JM-1232 L-838,417 Lirequinil (Ro41-3696) NS-2664 NS-2710 NS-11394 Pipequaline ROD-188 RWJ-51204 SB-205,384 SX-3228 TGSC01AA TP-003 TPA-023 TP-13 U-89843A U-90042 Viqualine Y-23684
Phenols	Fospropofol Propofol Thymol
Piperidinediones	Glutethimide Methyprylon Piperidione Pyrithyldione
Pyrazolopyridines	Cartazolate Etazolate ICI-190,622 Tracazolate
Quinazolinones	Afloqualone Cloroqualone Diproqualone Etaqualone Mebroqualone Mecloqualone Methaqualone Methylmethaqualone Nitromethaqualone SL-164
Volatiles/gases	Acetone Acetophenone Acetylglycinamide chloral hydrate Aliflurane Benzene Butane Butylene Centalun Chloral Chloral betaine Chloral hydrate Chloroform Cryofluorane Desflurane Dichloralphenazone Dichloromethane Diethyl ether Enflurane Ethyl chloride Ethylene Fluroxene Gasoline Halopropane Halothane Isoflurane Kerosine Methoxyflurane Methoxypropane Nitric oxide Nitrogen Nitrous oxide Norflurane Paraldehyde Propane Propylene Roflurane Sevoflurane Synthane Teflurane Toluene Trichloroethane (methyl chloroform) Trichloroethylene Vinyl ether
Others/unsorted	3-Hydroxybutanal α-EMTBL AA-29504 Avermectins (e.g., ivermectin) Bromide compounds (e.g., lithium bromide, potassium bromide, sodium bromide) Carbamazepine Chloralose Chlormezanone Clomethiazole DEABL Dihydroergolines (e.g., dihydroergocryptine, dihydroergosine, dihydroergotamine, ergoloid (dihydroergotoxine)) DS2 Efavirenz Etazepine Etifoxine Fenamates (e.g., flufenamic acid, mefenamic acid, niflumic acid, tolfenamic acid) Fluoxetine Flupirtine Hopantenic acid Lanthanum Lavender oil Lignans (e.g., 4-O-methylhonokiol, honokiol, magnolol, obovatol) Loreclezole Menthyl isovalerate (validolum) Monastrol Niacin Nicotinamide (niacinamide) Org 25,435 Phenytoin Propanidid Retigabine (ezogabine) Safranal Seproxetine Stiripentol Sulfonylalkanes (e.g., sulfonmethane (sulfonal), tetronal, trional) Terpenoids (e.g., borneol) Topiramate Valerian constituents (e.g., isovaleric acid, isovaleramide, valerenic acid, valerenol) Unsorted benzodiazepine site PAMs: MRK-409 (MK-0343) TCS-1105 TCS-1205
See also: Receptor/signaling modulators • GABA receptor modulators

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niacin

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Contents

Dietary reference intake

Food sources

Deficiency

Medical uses

Abnormal lipids

Treatment of deficiency

Contraindications

Side effects

Facial flushing

Gastrointestinal and hepatic

Metabolic

Other

In pregnancy

Pharmacology

Pharmacodynamics

Pharmacokinetics

Biosynthesis

Physical and chemical properties

Laboratory synthesis

Preparations

Nicotinic acid

Extended release

Inositol hexanicotinate

Nicotinamide

History

Research

References

External links

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★リンクテーブル★

「ナイアシン」

臨床関連

「ピルビン酸デヒドロゲナーゼ」

概要

反応

補酵素

臨床関連

不足

「ニコチン酸」

概念

臨床関連

参考

「pertain」

「ビタミンB」

「niacinamide」

「xanthinol niacinate」