Inositol niacinate targets the cardiovascular system, mediating vasodilatory, lipid-lowering, and fibrinolytic effects. Like other niacins, it acts as a vasodilator. It is a source of niacin, which is released through hydrolysis in the body. Niacin is known to have lipid-lowering effects by inhibiting the production of VLDL and LDL cholesterol.

Inositol niacinate has vasodilatory effects. It has the effect of lowering cholesterol and expanding peripheral blood vessels. It does not significantly improve triglyceride levels in mice induced by biphenyl esters. Its effects are mediated through the release of niacin, which has well-characterized pharmacological activities.

Inositol niacinate has vasodilatory effects and can be used in research on peripheral arterial disease, showing efficacy when taken orally. It has the effect of lowering cholesterol and expanding peripheral blood vessels, making it useful for the treatment of hypercholesterolemia and atherosclerosis. Compared to free niacin, inositol niacinate causes less flushing.

Inositol niacinate does not have a typical enzyme/receptor binding assay. Its activity is assessed based on its ability to release niacin and its effects on lipid metabolism and vasodilation. The compound's effects on cholesterol levels and vascular function can be measured in various in vitro and in vivo models.

Cellular assays for Inositol niacinate involve treating cells with the compound and measuring its effects on lipid metabolism, such as cholesterol synthesis or uptake. Its effects on vascular smooth muscle cells can be assessed by measuring vasodilation or changes in calcium signaling.

In vivo animal experiments for Inositol niacinate would involve administering the compound to animal models of hypercholesterolemia or atherosclerosis to assess its lipid-lowering and vasodilatory effects. Its effects on cholesterol levels, plaque formation, and vascular function would be evaluated. However, specific in vivo data is not detailed in the provided sources.

Absorption, Distribution and Excretion
The gastrointestinal absorption rate of inositol hexanicotinic acid ester varies considerably. On average, 70% of the oral dose is absorbed intact from the stomach and upper small intestine into the bloodstream. Peak serum nicotinic acid concentrations are reached approximately 6–10 hours after oral administration. At low concentrations, the absorption of nicotinic acid and nicotinamide is primarily mediated by sodium-dependent facilitated diffusion. At high concentrations, passive diffusion dominates, with 3–4 g of nicotinic acid almost completely absorbed. Unabsorbed nicotinic acid inositol can be detected in feces. The mean volume of distribution (Vd) after intravenous injection of 50 mg/kg nicotinic acid inositol in rats was 1051 ± 250 mL/kg. The mean clearance rate after intravenous injection of 50 mg/kg nicotinic acid inositol in rats was 65.4 ± 19 mL/min/kg. Metabolism/Metabolites Nicotinic acid inositol is hydrolyzed by plasma esterases, continuously releasing free nicotinic acid and inositol. The process took over 48 hours, during which it was found that the enzymatic hydrolysis of inositol hexanicotinate in the blood was slower at the first ester bond than at subsequent ester bonds. Each step of the sequential hydrolysis of inositol nicotinate produces one nicotinic acid molecule, ultimately resulting in six nicotinic acid molecules and one inositol moiety.

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Biological Half-Life
The average elimination half-life for a healthy adult is approximately one hour.
Inositol niacinate has a molecular weight of 810.72 g/mol and a molecular formula of C42H42N6O18. It is a synthetic ester derived from inositol and nicotinic acid. The compound is a niacin preparation that releases free niacin through hydrolysis in the body. It is typically used as a research reagent.

Toxicological data for Inositol niacinate is characteristic of niacin preparations. Common adverse effects include flushing, itching, and gastrointestinal disturbances. However, inositol niacinate causes less flushing compared to free niacin. Its safety has been evaluated in clinical studies for the treatment of hypercholesterolemia and atherosclerosis.

[1]. A systematic review and economic evaluation of cilostazol, naftidrofuryl oxalate, pentoxifylline and inositol nicotinate for the treatment of intermittent claudication in people with peripheral arterial disease. NIHR Health Technology Assessment programme: Executive Summaries.

Inositol hexanicotinate is a type of inositol nicotinate whose function is related to niacin. Inositol nicotinate, also known as inositol hexanicotinate/hexanicotinate or "non-flushing niacin," is a nicotinate and vasodilator. It is used as a source of niacin (vitamin B3) in dietary supplements; 1 gram (1.23 mmol) of inositol hexanicotinate hydrolyzes to produce 0.91 grams of niacin and 0.22 grams of inositol. Niacin exists in various forms, including niacin, nicotinamide, and other derivatives such as inositol nicotinate. Compared to other vasodilators, it reduces flushing due to the slower breakdown of its metabolites and inositol. Niacin plays a crucial role in many important metabolic processes and has been used as a lipid-lowering drug. Inositol nicotinate is marketed in Europe under the brand name Hexopal for the treatment of severe intermittent claudication and Raynaud's phenomenon. Inositol nicotinate is a niacin preparation that does not contain free niacin, but it can release free niacin through hydrolysis in the body. Compared to the use of free niacin, the use of inositol niacinate causes less flushing. Pharmacological Indications As a dietary supplement, it provides niacin. Its potential benefits on blood lipids have been studied. In Europe, inositol hexanicotinate is a patented drug called Hexopal, used to treat symptoms of severe intermittent claudication and Raynaud's phenomenon. Mechanism of Action Inositol niacinate and other niacin derivatives directly and non-competitively inhibit the microsomal enzyme diacylglycerol acyltransferase 2 (DGAT2), which is responsible for fatty acid esterification to triglycerides, thereby reducing triglyceride synthesis and the secretion of atherosclerotic lipoproteins in the liver. Inhibition of triglyceride synthesis leads to accelerated degradation of apolipoprotein B in hepatocytes and reduced secretion of very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) particles. Niacin also inhibits the expression of hepatic β-chain adenosine triphosphate synthase, thereby inhibiting the clearance or uptake of high-density lipoprotein-apolipoprotein AI. Studies have shown that niacin can improve the redox state of vascular endothelial cells, thereby inhibiting oxidative stress and vascular inflammation genes or key cytokines involved in atherosclerosis. As a ligand for G protein-coupled receptors 109A (HCAR2/HM74A) and 109B (HCAR3/HM74), it mediates the anti-lipolysis and lipid-lowering effects of niacin. Niacin-mediated reductions in the GPR109A signaling pathway expressed on adipocytes and G(i) protein-mediated decreases in cAMP levels lead to reduced lipolysis, fatty acid mobilization, and triglyceride synthesis. Compared to other niacin molecules, inositol nicotinate's effect on increasing prostaglandin D2/E2 activity by acting on GPR109A expressed on skin and macrophages is considered weaker because of its sustained-release effect, resulting in less flushing.
Inositol niacinate (myo-Inositol hexanicotinate) is a vasodilatory and lipid-lowering agent used for the treatment of hypercholesterolemia and atherosclerosis. It is a niacin preparation that releases free niacin through hydrolysis in the body, causing less flushing than free niacin. It is available from various chemical suppliers for research purposes.

C42H30N6O12

810.73

810.192

6556-11-2

3720

White to off-white solid powder

1.5±0.1 g/cm3

897.0±65.0 °C at 760 mmHg

254-256ºC

496.3±34.3 °C

0.0±0.3 mmHg at 25°C

1.675

6.37

0

18

18

60

1210

0

MFZCIDXOLLEMOO-UHFFFAOYSA-N

InChI=1S/C42H30N6O12/c49-37(25-7-1-13-43-19-25)55-31-32(56-38(50)26-8-2-14-44-20-26)34(58-40(52)28-10-4-16-46-22-28)36(60-42(54)30-12-6-18-48-24-30)35(59-41(53)29-11-5-17-47-23-29)33(31)57-39(51)27-9-3-15-45-21-27/h1-24,31-36H

[2,3,4,5,6-pentakis(pyridine-3-carbonyloxy)cyclohexyl] pyridine-3-carboxylate

NSC-49506; NSC 49506; Inositol niacinate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO :< 1 mg/mL

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.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*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).

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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)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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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).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)