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(FOH-lick acid/NICK-oh-TIN-uh-mide/zink)


USES: This combination medication is used to treat certain types of acne (e.g., acne vulgaris, acne rosacea) or other irritated skin conditions. People who have low levels of nicotinamide, zinc, or folic acid in their body may develop, or be at an increased risk of developing, these types of skin conditions.

HOW TO USE: Take this medication by mouth usually once or twice daily, or take as directed by your doctor. Taking this product with food may help to reduce any nausea that may occur due to this medicine. Consult your pharmacist.

SIDE EFFECTS: Nausea or vomiting may occur. If any of these effects persist or worsen, notify your doctor. Tell your doctor immediately if any of these serious side effects occur: stomach pain, yellowing eyes and skin, dark urine, fatigue, fever. An allergic reaction to this product is unlikely, but seek immediate medical attention if it occurs. Symptoms of an allergic reaction include: rash, itching, swelling, dizziness, trouble breathing. If you notice other effects not listed above, contact your doctor or pharmacist.

PRECAUTIONS: Tell your doctor your medical history, especially of: liver problems (e.g., jaundice), diabetes, blood problems (e.g., pernicious anemia), any allergies. This medication should be used only when clearly needed during pregnancy. Discuss the risks and benefits with your doctor. It is not known whether this drug passes into breast milk. Consult your doctor before breast-feeding.

DRUG INTERACTIONS: Tell your doctor of all prescription and nonprescription medication you may use, especially: certain anti- seizure medicine (e.g., carbamazepine, primidone), quinolone antibiotics (e.g., ciprofloxacin, levofloxacin), tetracycline antibiotics (e.g., doxycycline, minocycline), vitamin products. Do not start or stop any medicine without doctor or pharmacist approval.

OVERDOSE: If overdose is suspected, contact your local poison control center or emergency room immediately.

NOTES: Do not share this medication with others. Laboratory and/or medical tests may be performed to monitor your progress.

MISSED DOSE: If you miss a dose, use it as soon as you remember. If it is near the time of the next dose, skip the missed dose and resume your usual dosing schedule. Do not double the dose to catch up.

STORAGE: Store at room temperature between 59 and 86 degrees F (15 to 30 degrees C) away from light and moisture.


Nicotinamide (niacinamide) is one of the two principal forms of the B-complex vitamin niacin (see Niacin). The term niacin is used as a collective term to refer to both nicotinamide and nicotinic acid, the other principal form of niacin, or the term is used synonymously with nicotinic acid. Nicotinamide and nicotinic acid have identical vitamin activities, but they have very different pharmacological activities.

Nicotinamide, via its major metabolite NAD++ (nicotinamide adenine dinucleotide), is involved in a wide range of biological processes, including the production of energy, the synthesis of fatty acids, cholesterol and steroids, signal transduction and the maintenance of the integrity of the genome. Nicotinic acid, in pharmacological doses, is used as an antihyperlipidemic agent. It also causes vasodilation of cutaneous blood vessels resulting in the so-called niacin flush. Nicotinamide in pharmacological doses does not have antihyperlipidemic activity, nor does it cause a niacin-flush. There is evidence, however, that pharmacological doses of nicotinamide may prevent type 1 diabetes mellitus. And, interestingly, pyrazinamide, an important drug in the treatment of tuberculosis, is an analogue of and shares the same biochemical mechanism with nicotinamide.

Nicotinamide, in addition to being known as niacinamide, is also known as 3-pyridinecarboxamide, pyridine-3-carboxamide, nicotinic acid amide, vitamin B3 and vitamin PP. Its molecular formula is C6H6N2O and its molecular weight is 122.13 daltons and the structural formula is:


Nicotinamide is the principal form of niacin used in nutritional supplements and in food fortification. See also Niacin (Nicotinic Acid).

Nicotinamide may have anti-diabetogenic activity in some. It may also have antioxidant, anti-inflammatory and anticarcinogenic activities. Nicotinamide has putatitive activity against osteoarthritis and granuloma annulare.

Nicotinamide is being investigated as an agent for the possible prevention or delaying of the onset of type 1 diabetes mellitus (insulin-dependent diabetes mellitus or IDDM). The rationale for using nicotinamide to prevent type 1 diabetes mellitus is derived from human and animal studies as well as in vitro investigations. Nicotinamide has been found to prevent diabetes in alloxan- and streptozotocin-treated mice and rats and in non-obese diabetic (NOD) mice. In vitro studies have shown that nicotinamide can prevent macrophage- or interleukin-1beta-induced beta-cell damage. An intervention study in New Zealand using nicotinamide treatment showed a 50% reduction in the development of IDDM over a five-year period.

The mechanism of the possible anti-diabetogenic activity of nicotinamide is not well understood. The pathogenesis of IDDM involves the autoimmune destruction of beta-cells, which is accompanied by the appearance of beta-cell specific antibodies, such as islet cell antibodies (ICA) and antibodies to glutamic acid decarboxylase (GAD), many years before the onset of the disease. Macrophages and T lymphocytes are the first cells to appear in the islets of the pancreas during the development of autoimmune diabetes. It is thought that cytokines released by macrophages/monocytes, such as interleukin (IL)-12 and tumor necrosis factor (TNF)-alpha, might play a role in early beta-cell damage. IL-12 may play a role in the initiation of the autoimmune process by enhancing T helper 1 lymphocyte (Th1) responses. Nicotinamide has been shown to decrease the production of IL-12 and TNF-alpha in cultures of whole blood from prediabetic and diabetic subjects and also in healthy controls. Inhibition of IL-12 production by nicotinamide could play an important role in the modulation of the immune response leading to IDDM. Further, since the cytokine-inhibitory activity was observed in healthy controls, as well as in prediabetic and diabetic subjects, nicotinamide may have application in other autoimmune disorders.

Nicotinamide has been demonstrated, in one study, to affect glucose tolerance and insulitis in NOD mice, slowing down diabetes progression. In this study, nicotinamide decreased MHC class II expression (but not MHC class I), enhanced intercellular adhesion molecule-1 (ICAM-1) expression, counteracted the fall of superoxide dismutase (observed in untreated NOD mice) and increased the levels of interleukin (IL)-4, a T helper 2 lymphocyte (Th2) protective cytokine.

The anti-diabetogenic effect of nicotinamide may be due, in part, to an increase in the pool size of NAD++ in beta-cells. NAD++ is the principal metabolite of nicotinamide. It appears that the pool size of NAD++ in beta-cells in pre-diabetics and diabetics is significantly reduced. Damage and destruction of beta-cells may occur via oxidative stress. Increased levels of reactive oxygen species in beta-cells may result in, among other things, oxidative damage to DNA resulting in DNA strand breaks. The enzyme poly(ADP-ribose)polymerase or PARP is believed to play a role in DNA repair. PARP uses NAD++ as its substrate. In the context of a reduced level of NAD++, PARP activity may essentially use most of the cellular NAD++. This could result in cellular apoptosis. Nicotinamide is an inhibitor of PARP. It also has antioxidant activity and, of course, is metabolized to NAD++. All of these effects may play some role in the possible anti-diabetogenic action of nicotinamide.

Nicotinamide has been shown to have antioxidant activity. In vitro, it has been found to inhibit protein oxidation and lipid peroxidation. It has also been found to inhibit reactive oxygen species-induced apoptosis, to inhibit phagocytic generation of reactive oxygen species, to scavenge reactive oxygen species and to inhibit the oxidative activity of nitric oxide.

Nicotinamide has demonstrated a number of anti-inflammatory activities. Nicotinamide has been shown to inhibit lipopolysaccharide-induced TNF-alpha in the mouse, in a dose-dependent manner. It is thought that this inhibition of TNF-alpha is mediated via inhibition, at the gene transcription level, of NF-Kappa B, which in turn inhibits TNF-alpha. Nicotinamide has also been shown to decrease the production of IL-12 and TNF-alpha in cultures of whole blood from prediabetic and diabetic subjects and also in healthy subjects.

Niacin deficiency has been found to inhibit DNA repair in cell culture models. NAD++ is the substrate for PARP, an enzyme thought to be involved in DNA repair. Extensive damage to DNA may result in depletion of NAD++ secondary to its use by PARP. Depletion of NAD+ may trigger cellular apoptosis. DNA repair by PARP, as well as its possible role in apoptosis, may contribute to protection against carcinogenesis. These mechanisms may account, in part, for the possible anticarcinogenic activity of nicotinamide. Nicotinamide, via NAD++, modulates the expression of the p53 tumor suppressor protein in human breast, lung, skin and lung cells. This is another mechanism for nicotinamide's possible anticarcinogenic activity.

A pilot study suggests that nicotinamide may be beneficial in some with osteoarthritis. The mechanism of this putative activity is unknown. The mechanism of the putative activity of nicotinamide in granuloma annulare is also unknown.

Nicotinamide is efficiently absorbed from the gastrointestinal tract. At low doses, absorption is mediated via sodium-dependent facilitated diffusion. Passive diffusion is the principal mechanism of absorption at higher doses. Doses of up to three to four grams of nicotinamide are almost completely absorbed. Nicotinamide is transported via the portal circulation to the liver and via the systemic circulation to the various tissues of the body. Nicotinamide enters most cells by passive diffusion and enters erythrocytes by facilitated transport.

Nicotinamide is metabolized to NAD++ which in turn has a number of metabolic opportunities, including the formation of nicotinamide, NADP++ (nicotinamide adenine dinucleotide phosphate), NMN (nicotinamide 5'-mononucleotide), cyclic ADP-ribose and NAADP (nicotinic acid dinucleotide phosphate). NAD++ also serves as the substrate for mono(ADP-ribosyl)ation and poly(ADP-ribosyl)ation. Poly(ADP-ribosyl)ation is catalyzed by PARP. Nicotinamide may be converted to nicotinic acid via the enzyme nicotinamidase.

In the liver, the principal catabolic products of high-dose nicotinamide are N'-methylnicotinamide, N'-methyl-5-carboxamide-2-pyridone, N'-methyl-5-carboxamide-4-pyridone and nicotinamide-N-oxide. High-dose nicotinamide is excreted in the urine as unchanged nicotinamide, N'-methylnicotinamide, N'-methyl-5-carboxamide-2-pyridone, N'-meth- yl-5-carboxamide-4-pyridone and nicotinamide-N-oxide.

Nicotinamide, unlike nicotinic acid, does not have significant effects on lipids, but it has been shown to be useful in some with type 1 (insulin-dependent) diabetes. There is preliminary evidence it might help some with generalized granuloma annulare and osteoarthritis. There is little evidence that it is helpful in rheumatoid arthritis or schizophrenia. There is a suggestion that it might aid in some cancer therapies. There is little evidence that it is useful in tinnitus.

Nicotinamide was shown to protect the non-obese diabetic (NOD) mouse from type 1 (IDDM) diabetes if given early enough and at high enough doses. Nicotinamide might similarly intervene in human type 1 diabetes as evidenced, among other things, by its observed ability to protect isolated islets of Langerhans in vitro from various toxic agents. In vitro experiments also showed that nicotinamide could reduce beta cell impairment and death caused by macrophages and exposure to various cytokines involved in this autoimmune disease.

Since nicotinamide has not been shown to have significant, prolonged effects when introduced after the onset of type 1 diabetes, its efficacy has been researched as an interventive therapy. It shows some ability to extend the remission phase when *****istered to subjects newly diagnosed with the disease. During the remission phase, the need for exogenous insulin is decreased or obliterated, but insulin-dependence reasserts itself, usually within one year despite nicotinamide supplementation. On the other hand, nicotinamide appears to be far more effective as a preventive.

In one 5-year intervention study, nicotinamide was *****istered prior to the clinical onset of IDDM. Using antibody markers that predict the onset of IDDM within 5 years, 150 young subjects were selected to receive nicotinamide at a dose of 1.2 grams per square meter of body surface area daily. It was concluded that nicotinamide supplementation reduced the expected incidence of IDDM 50% over a 5-year period. A much larger multi-center intervention study is now underway.

There is one recent single-blind, placebo-controlled study indicating that nicotinamide improves insulin secretion and metabolic control in lean type 2 diabetic patients with secondary failure to sulfonylureas. Followup is needed.

There is a case study showing pronounced improvement in a patient with generalized granuloma annulare treated with high-dose (1,500 milligrams daily) niacinamide for six months. This patient's disease had previously resisted treatment with topical adrenal steroids, oral erythromycin and oral zinc.

A recent double-blind, placebo-controlled, pilot study examined the effect of nicotinamide in subjects with osteoarthritis. In the study, 72 subjects with osteoarthritis were randomly assigned to receive nicotinamide (500 milligrams six times per day) or placebo. The study lasted 12 weeks. Subjects who received nicotinamide reduced their non-steroidal anti-inflammatory (NSAID) medication by 13% compared with those in the placebo group. Pain levels were no different in the two groups. Nicotinamide reduced the sedimentation rate by 22% and increased joint mobility by 22% over controls. Followup is needed.

Some preliminary evidence suggests that nicotinamide may increase the irradiation response of experimental tumors. More research is needed in this area.

Nicotinamide produced effects no better than placebo when used in a double-blind trial involving 48 subjects with tinnitus.

Nicotinamide is contraindicated in those hypersensitive to any component of a nicotinamide-containing preparation.

High-dose nicotinamide (doses greater than 500 milligrams/day) is contraindicated in those with liver disease and in those with active peptic ulcer disease.

Pregnant women and nursing mothers should avoid supplemental doses of nicotinamide greater than the U.S. RDA (20 milligrams/day), unless higher doses are prescribed by their physicians.

The use of nicotinamide for any medical indication requires medical supervision.

Those with a history of peptic ulcer disease, gastritis, liver disease, gallbladder disease, diabetes and gout, should exercise caution in the use of high-dose nicotinamide.

In contrast to nicotinic acid, nicotinamide does not cause flushing and has only very rarely been associated with diabetogenic effects. There are rare reports of elevations in liver tests and liver damage, including jaundice and parenchymal liver cell injury. These reports were in those using very high doses of nicotinamide (10 grams or greater, daily).

Adverse reactions in those using high-dose nicotinamide, include nausea, vomiting, diarrhea, headache and dizziness.

Carbamazepine: Concomitant use of nicotinamide and carbamazepine may decrease carbamazepine clearance.

Nicotinamide overdosage is not reported in the literature.

Nicotinamide is the form of niacin which is typically used for nutritional supplementation. It is also the form of niacin used in food fortification. It is available as a single ingredient product (immediate-release and sustained-release) and in multivitamin and multivitamin/multimineral products. Typical supplemental dosage ranges from 20 to 100 milligrams daily. Pre- and postnatal vitamin/mineral supplements typically deliver a dose of 20 milligrams daily.

Capsules 100 mg, 250 mg, 500 mg, 550 mg

Tablets 100 mg, 250 mg, 500 mg

Tablets, Extended Release 1000 mg, 1500 mg

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