| Size | Price | |
|---|---|---|
| 500mg | ||
| 1g | ||
| Other Sizes |
| Targets |
Niacin binds to the G-protein coupled receptor GPR109A (also known as HM74A, HCA2, niacin receptor), a Gi-coupled receptor. Through this receptor, niacin increases arachidonic acid levels and prostaglandin synthesis, leading to cutaneous vasodilation and flushing. Niacin also decreases surface expression of hepatic ATP synthase β (reducing HDL catabolism and increasing serum HDL levels) and inhibits hepatic diacylglycerol acyltransferase-2 (inhibiting triglyceride synthesis and decreasing VLDL/LDL secretion).
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|---|---|
| ln Vitro |
Niacin hydrochloride (0-900 μM, 42 hours) alters the expression of genes linked to lipid metabolism and apoptosis, and it dramatically raises GSH levels and lowers ROS levels [1]. Small dosages of niacin hydrochloride (0–40 μM, 24 hours) can suppress cancer invasive activity, but not proliferation [2].
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| ln Vivo |
Male C57BL/6 mice are given subcutaneous injections of niacin hydrochloride (3–300 mg/kg once) and within minutes, vasodilation is induced in a dose-dependent manner [3].
|
| Cell Assay |
RT-PCR[1]
Cell Types: cumulus cells and oocytes of prepubertal sows Tested Concentrations: 600 μM Incubation Duration: 42 hrs (hours) Experimental Results: Up-regulated the relative expression of anti-apoptotic gene BCL2 and lipid metabolism gene ACACA, down-regulated the pro-apoptotic gene Apoptosis gene BAX. Cell proliferation experiment [2] Cell Types: AH109A rat ascites liver cancer cell line Tested Concentrations: 0-40 μM Incubation Duration: 24 hrs (hours) Experimental Results: 2.5 μM to 40 μM has no effect on AH109A cell proliferation, but inhibits cell invasion. |
| Animal Protocol |
Animal/Disease Models: Male C57BL/6 mice [3]
Doses: 3-300 mg/kg Route of Administration: subcutaneous injection; Experimental Results:Induced vasodilation in a dose-dependent manner. |
| ADME/Pharmacokinetics |
Niacin exhibits rapid and complete absorption from the gastrointestinal tract with oral bioavailability approaching 100% for immediate-release formulations (60-76% for sustained-release formulations compared to immediate-release). Peak plasma concentrations are reached 30-60 minutes after oral administration. The drug is widely distributed throughout body tissues including liver, kidney, and adipose tissue, and is excreted into breast milk. Plasma protein binding is less than 20%. The elimination half-life is short, approximately 15-45 minutes. Niacin is metabolized in the liver primarily to nicotinuric acid, N-methylnicotinamide, and pyridone derivatives. Approximately two-thirds of a dose is excreted unchanged in urine; excess amounts are predominantly excreted renally.
For sustained-release preparations, the unique release profile results in metabolism primarily via the amidation pathway, resulting in lower flushing incidence compared to immediate-release formulations. In animal studies (Mtmr2 KO mice), niacin-SR (960 mg/kg, oral) compared to pure niacin (120 mg/kg, i.p.) and pure niacin (240 mg/kg, oral) were evaluated for their pharmacokinetic profiles in nerve tissue. |
| Toxicity/Toxicokinetics |
Niacin at pharmacological doses (typically 500-3000 mg/day) causes several predictable adverse effects. Flushing (cutaneous vasodilation with redness, warmth, and itching) is the most common side effect, occurring in up to 20-50% of patients, mediated by prostaglandin release, and typically subsides with continued use. Flushing is more common with immediate-release preparations and can be minimized by taking niacin after meals, starting at low doses (e.g., 50 mg three times daily) and increasing slowly, or pre-treatment with aspirin (325 mg) 30-45 minutes before niacin.
Hepatotoxicity: At daily doses exceeding 500 mg, up to 20% of patients experience asymptomatic transient serum aminotransferase elevations, though rarely exceeding 3 times the upper limit of normal. Serious hepatotoxicity is uncommon but has been reported, particularly with sustained-release formulations; cases may present with jaundice, nausea, vomiting, fatigue, and elevated transaminases; liver biopsy may show centrilobular necrosis with minimal inflammation. Monitoring of liver function tests (ALT, AST) is recommended every 6-8 weeks until the dose is stabilized.
Other adverse effects: Hyperglycemia (blood glucose elevation) and worsening of diabetes mellitus, hyperuricemia and precipitation of gout, gastrointestinal complaints (dyspepsia, nausea), myopathy (muscle toxicity) risk increased when combined with statins, and rarely blurred vision, jaundice, and abdominal discomfort. Contraindications: Known hypersensitivity, active liver disease, active peptic ulcer disease, arterial bleeding, and in pregnant or lactating women (use with caution). The drug may cause false-positive results for urinary catecholamines (fluorometric method) and urinary glucose (copper reduction method). |
| References |
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| Additional Infomation |
A water-soluble B vitamin found in various animal and plant tissues. The human body needs it to synthesize the coenzymes NAD and NADP. It has therapeutic effects on pellagra, vasodilators, and lipid-lowering agents.
Niacin (nicotinic acid, vitamin B3, pyridine-3-carboxylic acid) has a molecular formula of C6H5NO2, molecular weight 123.11, and melting point 236.6°C. It is a white crystalline powder, soluble in water (16 mg/mL), ethanol (10 mg/mL), and DMSO (25 mg/mL). Niacin was first discovered in 1937 by Conrad Elvehjem, and the name “niacin” was derived from “nicotinic acid + vitamin” to avoid association with nicotine. Niacin deficiency causes pellagra, characterized by the three D‘s: dermatitis, diarrhea, and dementia, which can be fatal if untreated. As a vitamin, it is found in dried yeast, liver, red meat, poultry, fish, legumes, and whole-grain or enriched cereal products. At pharmacological doses (much higher than nutritional requirements, typically 1-3 g/day), niacin is FDA-approved for dyslipidemia, including primary hyperlipidemia and mixed dyslipidemia. It is available in immediate-release (over-the-counter), sustained-release (prescription), and extended-release (prescription) formulations. Immediate-release formulations are often available as over-the-counter dietary supplements. The receptor GPR109A (HCA2, HM74A) is the primary molecular target for niacin’s pharmacological effects. The characteristic flushing side effect is prostaglandin-mediated and can be reduced but not eliminated by aspirin pre-treatment. Evidence regarding whether niacin reduces risk of coronary artery disease and stroke is mixed; some large clinical trials have not demonstrated additional benefit when added to statin therapy. |
| Molecular Formula |
C6H5NO2.HCL
|
|---|---|
| Molecular Weight |
159.57034
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| Exact Mass |
159.009
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| Elemental Analysis |
C, 45.16; H, 3.79; Cl, 22.22; N, 8.78; O, 20.05
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| CAS # |
636-79-3
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| Related CAS # |
Niacin;59-67-6
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| PubChem CID |
71558
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| Appearance |
Typically exists as solid at room temperature
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| Boiling Point |
292.5ºC at 760 mmHg
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| Melting Point |
236.6ºC
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| Flash Point |
130.7ºC
|
| LogP |
1.581
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| Hydrogen Bond Donor Count |
2
|
| Hydrogen Bond Acceptor Count |
3
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| Rotatable Bond Count |
1
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| Heavy Atom Count |
10
|
| Complexity |
114
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| Defined Atom Stereocenter Count |
0
|
| SMILES |
O=C(C1=NC=CC=C1)O.[H]Cl
|
| InChi Key |
IBTWUVRCFHJPKN-UHFFFAOYSA-N
|
| InChi Code |
InChI=1S/C6H5NO2.ClH/c8-6(9)5-2-1-3-7-4-5;/h1-4H,(H,8,9);1H
|
| Chemical Name |
pyridine-3-carboxylic acid;hydrochloride
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| Synonyms |
Niacin hydrochloride; 636-79-3; 3-Pyridinecarboxylic acid, hydrochloride; NSC-15010; 6C7S2KVE4G;
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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|---|---|
| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 6.2668 mL | 31.3342 mL | 62.6684 mL | |
| 5 mM | 1.2534 mL | 6.2668 mL | 12.5337 mL | |
| 10 mM | 0.6267 mL | 3.1334 mL | 6.2668 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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