Twinlab B-50
Twinlab B-50 Uses, Dosage, Side Effects, Food Interaction and all others data.
A water-soluble, enzyme co-factor present in minute amounts in every living cell. It occurs mainly bound to proteins or polypeptides and is abundant in liver, kidney, pancreas, yeast, and milk.
Biotin is a water-soluble B-complex vitamin which is composed of an ureido ring fused with a tetrahydrothiophene ring, which attaches a valeric acid substituent at one of its carbon atoms. Biotin is used in cell growth, the production of fatty acids, metabolism of fats, and amino acids. It plays a role in the Kreb cycle, which is the process in which energy is released from food. Biotin not only assists in various metabolic chemical conversions, but also helps with the transfer of carbon dioxide. Biotin is also helpful in maintaining a steady blood sugar level. Biotin is often recommended for strengthening hair and nails. Consequenty, it is found in many cosmetic and health products for the hair and skin. Biotin deficiency is a rare nutritional disorder caused by a deficiency of biotin. Initial symptoms of biotin deficiency include: Dry skin, Seborrheic dermatitis, Fungal infections, rashes including erythematous periorofacial macular rash, fine and brittle hair, and hair loss or total alopecia. If left untreated, neurological symptoms can develop, including mild depression, which may progress to profound lassitude and, eventually, to somnolence; changes in mental status, generalized muscular pains (myalgias), hyperesthesias and paresthesias. The treatment for biotin deficiency is to simply start taking some biotin supplements. A lack of biotin in infants will lead to a condition called seborrheic dermatitis or "cradle cap". Biotin deficiencies are extremely rare in adults but if it does occur, it will lead to anemia, depression, hair loss, high blood sugar levels, muscle pain, nausea, loss of appetite and inflamed mucous membranes.
Inositol is a collection of nine different stereoisomers but the name is usually used to describe only the most common type of inositol, myo-inositol. Myo-inositol is the cis-1,2,3,5-trans-4,6-cyclohexanehexol and it is prepared from an aqueous extract of corn kernels by precipitation and hydrolysis of crude phytate. These molecules have structural similarities to glucose and are involved in cellular signaling. It is considered a pseudovitamin as it is a molecule that does not qualify to be an essential vitamin because even though its presence is vital in the body, a deficiency in this molecule does not translate into disease conditions. Inositol can be found as an ingredient of OTC products by Health Canada but all current product whose main ingredient is inositol are discontinued. By the FDA, inositol is considered in the list of specific substances affirmed as generally recognized as safe (GRAS).
Inositol can stimulate glucose uptake in skeletal muscle cells which allows the decrease in blood sugar levels. This effect is later seen as a reduction in urine glucose concentration and indicates a decrease in high blood sugar levels.
In PCOS, the administration of inositol has produced the remission of symptoms as well as a reduction in male hormone secretion, a regulation of the cholesterol level, and a more efficient fat breakdown which allow to a significant reduction on body mass and appetite.
Niacin is a preparation of Nicotinic acid. It is proven effective at lowering VLDL, LDL, total cholesterol and triglyceride levels while raising HDL levels. So Niacin has been prescriped for the treatment of cardiovascular disease particularly the hyperlipidemias.
Niacin is a B vitamin used to treat vitamin deficiencies as well as hyperlipidemia, dyslipidemia, hypertriglyceridemia, and to reduce the risk of myocardial infarctions. Niacin acts to decrease levels of very low density lipoproteins and low density lipoproteins, while increasing levels of high density lipoproteins. Niacin has a wide therapeutic window with usual oral doses between 500mg and 2000mg. Patients with diabetes, renal failure, uncontrolled hypothyroidism, and elderly patients taking niacin with simvastatin or lovastatin are at increased risk of myopathy and rhabdomyolysis.
Pantothenic acid, also called pantothenate or vitamin B5 (a B vitamin), is a water-soluble vitamin discovered by Roger J. Williams in 1919. For many animals, pantothenic acid is an essential nutrient as it is required to synthesize coenzyme-A (CoA), as well as to synthesize and metabolize proteins, carbohydrates, and fats. Pantothenic acid is the amide between pantoic acid and β-alanine and commonly found as its alcohol analog, the provitamin panthenol, and as calcium pantothenate. Small quantities of pantothenic acid are found in nearly every food, with high amounts in whole-grain cereals, legumes, eggs, meat, royal jelly, avocado, and yogurt. Pantothenic acid is an ingredient in some hair and skin care products. Only the dextrorotatory (D) isomer of pantothenic acid possesses biological activity. while the levorotatory (L) form may antagonize the effects of the dextrorotatory isomer.
Pantothenic acid is used in the synthesis of coenzyme A (CoA). CoA is thought to act as a carrier molecule, allowing the entry of acyl groups into cells. This is of critical importance as these acyl groups are used as substrates in the tricarboxylic acid cycle to generate energy and in the synthesis of fatty acids, cholesterol, and acetylcholine. Additionally, CoA is part of acyl carrier protein (ACP), which is required in the synthesis of fatty acids in addition to CoAs use as a substrate.
Pantothenic acid in the form of CoA is also required for acylation and acetylation, which, for example, are involved in signal transduction and enzyme activation and deactivation, respectively.
Riboflavin is a B vitamin. It can be found in certain foods such as milk, meat, eggs, nuts, enriched flour, and green vegetables. Riboflavin is frequently used in combination with other B vitamins in vitamin B complex products. Vitamin B complex generally includes vitamin B1 (thiamine), vitamin B2 (riboflavin), vitamin B3 (niacin/niacinamide), vitamin B5 (pantothenic acid), vitamin B6 (pyridoxine), vitamin B12 (cyanocobalamin), and folic acid. However, some products do not contain all of these ingredients and some may include others, such as biotin, para-aminobenzoic acid (PABA), choline bitartrate, and inositol.
Riboflavin is used for preventing low levels of riboflavin (riboflavin deficiency), cervical cancer, and migraine headaches. It is also used for treating riboflavin deficiency, acne, muscle cramps, burning feet syndrome, carpal tunnel syndrome, and blood disorders such as congenital methemoglobinemia and red blood cell aplasia. Some people use riboflavin for eye conditions including eye fatigue, cataracts, and glaucoma.
Other uses include increasing energy levels; boosting immune system function; maintaining healthy hair, skin, mucous membranes, and nails; slowing aging; boosting athletic performance; promoting healthy reproductive function; canker sores; memory loss, including Alzheimer's disease; ulcers; burns; alcoholism; liver disease; sickle cell anemia; and treating lactic acidosis brought on by treatment with a class of AIDS medications called NRTI drugs.
Riboflavin or vitamin B2 is an easily absorbed, water-soluble micronutrient with a key role in maintaining human health. Like the other B vitamins, it supports energy production by aiding in the metabolising of fats, carbohydrates, and proteins. Vitamin B2 is also required for red blood cell formation and respiration, antibody production, and for regulating human growth and reproduction. It is essential for healthy skin, nails, hair growth and general good health, including regulating thyroid activity. Riboflavin also helps in the prevention or treatment of many types of eye disorders, including some cases of cataracts.
Thiamine, in the form of thiamine pyrophosphate, is the coenzyme for decarboxylation of α-ketoglutaric acid. Thiamine deficiency affects the peripheral nervous system, the gastrointestinal tract, and the cardiovascular system. This vitamin is necessary for the optimal growth of infants and children. Thiamine is not stored in the body, and is regularly lost from tissues during short periods of deficiency. In order to maintain normal health, an adequate amount of thiamine is required every day. Deficiency of thiamine leads to fatigue, anorexia, gastrointestinal disturbance, tachycardia, irritability and neurological symptoms. Beriberi, a disease due to vitamin B1 deficiency, is common in alcoholics, in pregnant women receiving an inadequate diet, and in people with malabsorption syndrome, prolonged diarrhoea and hepatic disease.
Thiamine is well absorbed from the gastrointestinal tract and widely distributed throughout the body. Thiamine is rapidly absorbed from the upper small intestine. Thiamine is not stored in the body to any appreciable extent. Excess ingested thiamine appears in urine as intact thiamine or as pyrimidine, which arises from degradation of the thiamine molecule. The plasma half life of thiamine is 24 hours.
Thiamine is a vitamin with antioxidant, erythropoietic, cognition-and mood-modulatory, antiatherosclerotic, putative ergogenic, and detoxification activities. Thiamine has been found to protect against lead-induced lipid peroxidation in rat liver and kidney. Thiamine deficiency results in selective neuronal death in animal models. The neuronal death is associated with increased free radical production, suggesting that oxidative stress may play an important early role in brain damage associated with thiamine deficiency. Thiamine plays a key role in intracellular glucose metabolism and it is thought that thiamine inhibits the effect of glucose and insulin on arterial smooth muscle cell proliferation. Inhibition of endothelial cell proliferation may also promote atherosclerosis. Endothelial cells in culture have been found to have a decreased proliferative rate and delayed migration in response to hyperglycemic conditions. Thiamine has been shown to inhibit this effect of glucose on endothelial cells.
| Trade Name | Twinlab B-50 |
| Generic | Thiamine + Riboflavin + niacin + vitamin B + asam folat + vitamin B + Biotin + pantothenic acid + cholne bitartrate + inositol + PABA |
| Weight | 50mg, 50mg, 50mg, 650mg, 400mcg, 1250mcg, 50mcg, 50mg, 50mg, 50mg, 50mg |
| Type | Capsule |
| Therapeutic Class | |
| Manufacturer | PT Natural Nutrindo |
| Available Country | Indonesia |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Biotin is a B-complex vitamin found in many multivitamin products.
For nutritional supplementation, also for treating dietary shortage or imbalance.
Inositol is an ingredient found in a variety of nutritional products.
Inositol may be used in food without any limitation. As a drug, inositol is used as a nutrient supplement in special dietary foods and infant formula. As it presents a relevant role in ensuring oocyte fertility, inositol has been studied for its use in the management of polycystic ovaries. Inositol is also being researched for the treatment of diabetes, prevention of metabolic syndrome, aid agent for weight loss, treatment of depression, psychiatric disorder and anxiety disorder and for prevention of cancer.
Therapy with lipid-altering agents should be only one component of multiple risk factor intervention in individuals at significantly increased risk for atheroscleroticvascular disease due to hyperlipidemia. Niacin therapy is used for an adjunct to diet when the response to a diet restricted in saturated fat and cholesterol and other nonpharmacologic measures alone has been inadequate.
- Niacin is used to reduce elevated TC, LDL-C, Apo B and TG levels, and to increase HDL-C in patients with primary hyperlipidemia and mixed dyslipidemia.
- In patients with a history of myocardial infarction and hyperlipidemia, niacin is used to reduce the risk of recurrent nonfatal myocardial infarction.
- In patients with a history of coronary artery disease (CAD) and hyperlipidemia, niacin, in combination with a bile acid binding resin, is used to slow progression or promote regression of atherosclerotic disease.
- Niacin in combination with a bile acid binding resin is used to reduce elevated TC and LDL-C levels in adult patients with primary hyperlipidemia.
- Niacin is also used as adjunctive therapy for treatment of adult patients with severe hypertriglyceridemia who present a risk of pancreatitis and who do not respond adequately to a determined dietary effort to control them.
Pantothenic acid is a vitamin B5 found in various nutritional supplements.
Studied for the treatment of many uses such as treatment of testicular torsion, diabetic ulceration, wound healing, acne, obesity, diabetic peripheral polyneuropathy. It has also been investigated for its hypolipidemic effects and as cholesterol lowering agent.
Preventing and treating riboflavin deficiency and conditions related to riboflavin deficiency.
Cataracts, an eye disorder. People who eat more riboflavin as part of their diet seems to have a lower risk of developing cataracts. Also, taking supplements containing riboflavin plus niacin seems to help prevent cataracts.
High amounts of homocysteine in the blood (hyperhomocysteinemia). Some people are unable to convert the chemical homocysteine into the amino acid methionine. People with this condition, especially those with low riboflavin levels, have high amounts of homocysteine in the blood. Taking riboflavin for 12 weeks seems to reduce homocysteine levels by up to 40% in some people with this condition. Also, certain antiseizure drugs can increase homocysteine in the blood. Taking riboflavin along with folic acid and pyridoxine seems to lower homocysteine levels by 26% in people with high homocysteine levels due to antiseizure drugs.
Migraine headaches. Taking high-dose riboflavin (400 mg/day) seems to significantly reduce the number of migraine headache attacks. However, taking riboflavin does not appear to reduce the amount of pain or the amount of time a migraine headache lasts. Also, taking lower doses of riboflavin (200 mg/day) does not seem to reduce the number of migraine headache attacks.
Thiamine is specifically used in the treatment of the various manifestations of thiamine deficiency such as Beriberi and Wernick's encephalopathy, neuritis associated with pregnancy and pellagra. Supplementary Thiamine may be used prophylactically in conditions where there is low dietary intake or impaired gastro intestinal absorption of thiamine (e.g. alcohol) or where requirements are increased (pregnancy, carbohydrate rich diet).
Twinlab B-50 is also used to associated treatment for these conditions: Vitamin Deficiency, Nutritional supplementationAtherosclerosis, Mixed Dyslipidemias, Myocardial Infarction, Pellagra, Vitamin Deficiency, Primary Hyperlipidemia, Severe Hyperlipidemia, Dietary supplementationNutritional supplementationAriboflavinosis, Beriberi, Constipation, Functional Gastrointestinal Disorders, Joint Pain, Metabolic cardiomyopathy, Migraine, Neuralgia, Peripheral neuritis, Peripheral paralysis, Soreness, Muscle, Vitamin B complex deficiency, Vitamin B1 deficiency, Vitamin Deficiency, Wernicke's encephalopathy, Dietary and Nutritional Therapies, Nutritional supplementation, Vitamin supplementation, Dietary supplementationAnemia, B12 Deficiency Anemia, Beriberi, Cardiovascular Heart Disease caused by Thiamine Deficiency, Folic Acid Deficiency Anemia, Infantile Beriberi, Infection, Iron Deficiency (ID), Liver disorder, Neuritis caused by Pregnancy, Secondary anemia, Thiamine Deficiency, Vitamin Deficiency, Wernicke's encephalopathy, Nutritional supplementation, Vitamin supplementation, Dietary supplementation
How Twinlab B-50 works
Biotin is necessary for the proper functioning of enzymes that transport carboxyl units and fix carbon dioxide, and is required for various metabolic functions, including gluconeogenesis, lipogenesis, fatty acid biosynthesis, propionate metabolism, and catabolism of branched-chain amino acids.
The mechanism of action of inositol in brain disorders is not fully understood but it is thought that it may be involved in neurotransmitter synthesis and it is a precursor to the phosphatidylinositol cycle. The change that occurs in the cycle simulates when the postsynaptic receptor is activated but without activating the receptor. This activity provokes a fake activation which regulated the activity of monoamines and other neurotransmitters.
Reports have shown that insulin resistance plays a key role in the clinical development of PCOS. The presence of hyperinsulinemia can induce an excess in androgen production by stimulating ovaries to produce androgens and by reducing the sex hormone binding globulin serum levels. One of the mechanisms of insulin deficiency is thought to be related to a deficiency in inositol in the inositolphosphoglycans. The administration of inositol allows it to act as a direct messenger of the insulin signaling and improves glucose tissue uptake. This mechanism is extrapolated to its functions in diabetes treatment, metabolic syndrome, and weight loss.
In cancer, the mechanism of action of inositol is not fully understood. It is hypothesized that the administration of inositol increases the level of lower-phosphate inositol phosphates why can affect cycle regulation, growth, and differentiation of malignant cells. On the other hand, the formation of inositol hexaphosphate after administration of inositol presents antioxidant characteristics by the chelation of ferric ions and suppression of hydroxyl radicals.
Niacin performs a number of functions in the body and so has many mechanisms, not all of which have been fully described. Niacin can decrease lipids and apolipoprotein B (apo B)-containing lipoproteins by modulating triglyceride synthesis in the liver, which degrades apo B, or by modulating lipolysis in adipose tissue.
Niacin inhibits hepatocyte diacylglycerol acyltransferase-2. This action prevents the final step of triglyceride synthesis in hepatocytes, limiting available triglycerides for very low density lipoproteins (VLDL). This activity also leads to intracellular degradation of apo B and decreased production of low density lipoproteins, the catabolic product of VLDL.
Niacin also inhibits a high density lipoprotein (HDL) catabolism receptor, which increases the levels and half life of HDL.
Pantothenic acid is incorporated into COENZYME A and protects cells against peroxidative damage by increasing the level of GLUTATHIONE.
Binds to riboflavin hydrogenase, riboflavin kinase, and riboflavin synthase. Riboflavin is the precursor of flavin mononucleotide (FMN, riboflavin monophosphate) and flavin adenine dinucleotide (FAD). The antioxidant activity of riboflavin is principally derived from its role as a precursor of FAD and the role of this cofactor in the production of the antioxidant reduced glutathione. Reduced glutathione is the cofactor of the selenium-containing glutathione peroxidases among other things. The glutathione peroxidases are major antioxidant enzymes. Reduced glutathione is generated by the FAD-containing enzyme glutathione reductase.
It is thought that the mechanism of action of thiamine on endothelial cells is related to a reduction in intracellular protein glycation by redirecting the glycolytic flux. Thiamine is mainly the transport form of the vitamin, while the active forms are phosphorylated thiamine derivatives. Natural derivatives of thiamine phosphate, such as thiamine monophosphate (ThMP), thiamine diphosphate (ThDP), also sometimes called thiamine pyrophosphate (TPP), thiamine triphosphate (ThTP), and thiamine triphosphate (AThTP), that act as coenzymes in addition to their each unique biological functions.
Dosage
Twinlab B-50 dosage
Niacin can be administered as a single dose at bedtime, after a snack or meal and doses should be individualized according to patient response. Therapy with Niacin must be initiated at 500 mg in order to reduce the incidence and severity of side effects which may occur during early therapy.
Maintenance Dose: The daily dosage of Niacin should not be increased by more than 500 mg in any 4-week period. The recommended maintenance dose is 1000 mg (two 500 mg tablets or one 1000 mg tablet) to 2000 mg (two 1000 mg tablets or four 500 mg tablets) once daily at bedtime. Doses greater than 2000 mg daily are not recommended. Women may respond at lower Niacin doses than men.
Single-dose bioavailability studies have demonstrated that two of the 500 mg and one of the 1000 mg tablet strengths are interchangeable but three of the 500 mg and two of the 750 mg tablet strengths are not interchangeable.
Flushing of the skin may be reduced in frequency or severity by pretreatment with aspirin (up to the recommended dose of 325 mg taken 30 minutes prior to Niacin dose). Tolerance to this flushing develops rapidly over the course of several weeks. Flushing,pruritus, andgastrointestinaldistress are also greatly reduced by slowly increasing the dose of niacin and avoiding administration on an empty stomach. Concomitant alcoholic, hot drinks or spicy foods may increase the side effects of flushing and pruritus and should be avoided around the time of Niacin ingestion.
Equivalent doses of Niacin should not be substituted for sustained-release (modified-release, timed-release) niacin preparations or immediate-release (crystalline) niacin. Patients previously receiving other niacin products should be started with the recommended Niacin titration schedule, and the dose should subsequently be individualized based on patient response.
If Niacin therapy is discontinued for an extended period, reinstitution of therapy should include a titration phase.
For treating low levels of riboflavin (riboflavin deficiency) in adults: 5-30 mg of riboflavin (Vitamin B2) daily in divided doses.
For preventing migraine headaches: 400 mg of riboflavin (Vitamin B2) per day. It may take up to three months to get best results.
For preventing cataracts: a daily dietary intake of approximately 2.6 mg of riboflavin (Vitamin B2) has been used. A combination of 3 mg of riboflavin (Vitamin B2) plus 40 mg of niacin daily has also been used.
The daily recommended dietary allowances (RDAs) of riboflavin (Vitamin B2) are:
- Infants 0-6 months: 0.3 mg
- Infants 7-12 months: 0.4 mg
- Children 1-3 years: 0.5 mg
- Children 4-8 years: 0.6 mg
- Children 9-13 years: 0.9 mg
- Men 14 years or older: 1.3 mg
- Women 14-18 years: 1 mg
- Women over 18 years: 1.1 mg
- Pregnant women: 1.4 mg
- Breastfeeding women: 1.6 mg
Prophylaxis: 3 to 10 mg daily.
Mild chronic deficiency: 10 to 25 mg daily.
Severe deficiency: 200 to 300 mg daily.
Niacin tablets should be taken whole and should not be broken, crushed or chewed before swallowing.
Side Effects
Niacin is generally well tolerated; adverse reactions have been mild and transient.The most frequent advers effects were flushing, itching, pruritis, nausea and GI upset, jaundice ,hypotension, tachycardia, increased serum blood glucose and uric acid levels, myalgia.
Get emergency medical help if you have signs of an allergic reaction: hives; difficult breathing; swelling of your face, lips, tongue, or throat. Riboflavin may cause your urine to turn a yellow-orange color, but this is usually not a harmful side effect.
Vitamin B1 does not have adverse effects when given orally, but in a few fatal cases anaphylactic reactions have occurred after intravenous administration of large doses (400 mg) in sensitive patients, especially children, and in one case following an intramuscular dose of 125 mg. The risk of such reactions increases with repeated administration of the drug by parenteral route. Transient mild soreness may occur at the site of intramuscular administration
Toxicity
Prolonged skin contact may cause irritation.
Consumption of high doses of inositol is reported to only cause some gastrointestinal effects.
Overdose of niacin may present with severe prolonged hypotension. Patients experiencing an overdose should be treated with supportive measures which may include intravenous fluids.
The oral LD50 in the mouse is 3720mg/kg, in the rabbit is 4550mg/kg, in the rat is 7000mg/kg, and the dermal LD50 in the rat is >2000mg/kg.
No Tolerable Upper Level Intake (UL) has been established for the vitamin.
Thiamine toxicity is uncommon; as excesses are readily excreted, although long-term supplementation of amounts larger than 3 gram have been known to cause toxicity. Oral mouse LD50 = 8224 mg/kg, oral rat LD50 = 3710 mg/kg.
Precaution
Before instituting therapy with Niacin, an attempt should be made to control hyperlipidemia with appropriate diet, exercise, and weight reduction in obese patients and to treat other underlying medical problems. Patients with a past history of jaundice, hepatobiliary disease, or peptic ulcer should be observed closely during Niacin therapy. Frequent monitoring of liver function tests and blood glucose should be performed to ascertain that the drug is producing no adverse effects on these organ systems. Diabetic patients may experience a dose-related rise in glucose intolerance, the clinical significance of which is unclear. Diabetic or potentially diabetic patients should be observed closely. Adjustment of diet and/or hypoglycemic therapy may be necessary.
Caution should also be used when Niacin is used in patients with unstable angina or in the acute phase of MI, particularly when such patients are also receiving vasoactive drugs such as nitrates, calcium channel blockers or adrenergic blocking agents. Elevated uric acid levels have occurred with Niacin therapy, therefore use with caution in patients predisposed to gout. Niacin has been associated with small but statistically significant dose-related reductions in platelet count and increases in prothrombin time. Caution should be observed when Niacin is administered concomitantly with anticoagulants; prothrombin time and platelet counts should be monitored closely in such patients. Niacin has been associated with small but statistically significant, dose-related reductions in phosphorus levels (mean of -13% with 2000 mg). So phosphorus levels should be monitored periodically in patients at risk.
Interaction
Niacin may potentiate the effects of ganglionic blocking agents and vasoactive drugs resulting in postural hypotension. Concomitant aspirin may decrease the metabolic clearance of nicotinic acid. The clinical relevance of this finding is unclear. About 98% of available Niacin was bound to colestipol, with 10 to 30% binding to cholestyramine. These results suggest that 4 to 6 hours, or as great an interval as possible, should elapse between the ingestion of bile acid-binding resins and the administration of Niacin.
Rate and extent of absorption may be affected by propantheline bromide.
No hazardous drug interactions have been reported. Vitamin B1 acts synergistically with other vitamins of the B-complex group and its potential for causing adverse effects is considerably reduced.
Volume of Distribution
The pharmacokinetic profile of inositol was studied in preterm infants and the estimated volume of distribution was reported to be 0.5115 L/kg.
Data regarding the volume of distribution of niacin is not readily available.
Elimination Route
Systemic - approximately 50%
Inositol is absorbed from the small intestine. In patients with inositol deficiency, the maximal plasma concentration after oral administration of inositol is registered to be of 4 hours. Inositol is taken up by the tissues via sodium-dependent inositol co-transporter which also mediates glucose uptake. Oral ingestion of inositol is registered to generate a maximal plasma concentration of 36-45 mcg.
In patients with chronic kidney disease, the Cmax is 0.06µg/mL for a 500mg oral dose, 2.42µg/mL for a 1000mg oral dose, and 4.22µg/mL for a 1500mg oral dose. The Tmax is 3.0 hours for a 1000mg or 1500mg oral dose. The AUC is 1.44µg*h/mL for a 500mg oral dose, 6.66µg*h/mL for a 1000mg oral dose, and 12.41µg*h/mL for a 1500mg oral dose. These values did not drastically differ in patients requiring dialysis.
Dietary pantothenic acid is primarily in the form of CoA or ACP and must be converted into free pantothenic acid for absorption. CoA and ACP are hydrolyzed into 4'-phosphopantetheine which is then dephosphorylated into pantetheine and subsequently hydrolyzed again to free pantothenic acid by Pantetheinase in the intestinal lumen. Free pantothenic acid is absorbed into intestinal cells via a saturable, sodium-dependent active transport system with passive diffusion acting as a secondary pathway. As intake increases up to 10-fold absorption rate can decrease to as low as 10% due to transporter saturation.
Vitamin B2 is readily absorbed from the upper gastrointestinal tract.
Absorbed mainly from duodenum, by both active and passive processes
Half Life
The pharmacokinetic profile of inositol was studied in preterm infants and the estimated elimination half-life was reported to be of 5.22 hours.
The half life of niacin is 0.9h, nicotinuric acid is 1.3h, and nicotinamide is 4.3h.
66-84 minutes
Clearance
The pharmacokinetic profile of inositol was studied in preterm infants and the estimated clearance rate was reported to be 0.0679 L.kg/h.
Data regarding the clearance of niacin is not readily available.
Elimination Route
Most of the administered dose is excreted in urine.
69.5% of a dose of niacin is recovered in urine. 37.9% of the recovered dose was N-methyl-2-pyridone-5-carboxamide, 16.0% was N-methylnicotinamide, 11.6% was nicotinuric acid, and 3.2% was niacin.
Pregnancy & Breastfeeding use
Niacin cannot be used in pregnancy and lactation because of a lack of information.
Riboflavin is LIKELY SAFE for pregnant or breast-feeding women when taken in the amounts recommended. The recommended amounts are 1.4 mg per day for pregnant women and 1.6 mg per day in breast-feeding women. Riboflavin is POSSIBLY SAFE when taken by mouth in larger doses, short-term. Some research shows that riboflavin is safe when taken at a dose of 15 mg once every 2 weeks for 10 weeks.
The drug may be given safely to neonates, children, pregnant and lactating women and elderly patients.
Contraindication
Niacin is contraindicated in patients with a known hypersensitivity to Niacin or any component of this medication, significant or unexplained hepatic dysfunction, active peptic ulcer disease or arterial bleeding.
There is no absolute contraindication but the risk of anaphylaxis is increased by repeated parenteral administration. Mild allergic phenomena, such as sneezing or mild asthma are warning signs that further may give rise to anaphylactic shock. To avoid this possibility it is advisable to start a second course of injection with a dose considerably lower than that previously used. Because of the above, vitamin B1 injection should not be given intravenously except in the case of comatose patients. Once thiamine deficiency is corrected there is no need for parenteral administration or for the administration of amounts in excess of daily requirement.
Acute Overdose
Supportive measures should be undertaken in the event of an overdosage. Symptoms may include nausea, dizziness, itching, vomiting, upset stomach, and flushing
Storage Condition
Store at 15-30° C.
Thiamine injection should be protected from light and moisture.
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