D-Panthenol 1 mg, D-Panthenol 1 mg, Diastase 25 mg, Folic Acid 75 mcg, Folic Acid 75 mcg, Lactobacillus Sporogenes 25 mg, Niacinamide 15 mg, Papain 20 mg, Pyridoxine 0.5 mg, Riboflavin 2.5 mg, Simethicone 40 mg, Vitamin B1 1 mg, Vitamin B2 2.5 mg, Vitamin B6 0.5 mg Hard-gelatin capsules

Folic acid acts on megaloblastic bone marrow to produce a normoblastic marrow.

In man, an exogenous source of folate is required for nucleoprotein synthesis and the maintenance of normal erythropoiesis. Folic acid is the precursor of tetrahydrofolic acid, which is involved as a cofactor for transformylation reactions in the biosynthesis of purines and thymidylates of nucleic acids. Impairment of thymidylate synthesis in patients with folic acid deficiency is thought to account for the defective deoxyribonucleic acid (DNA) synthesis that leads to megaloblast formation and megaloblastic and macrocytic anemias.

Absorption — Folic acid is absorbed from the small intestine, primarily from the proximal portion. Folic acid appears in the plasma approximately 15 to 30 minutes after an oral dose; peak levels are generally reached within 1 hour.

Distribution — Folic acid as well as its physiologically active metabolite, L-5-methyl tetrahydro folate (L-5-MTHF), can be bound to plasma proteins when entering the systemic circulation. The fraction of folic acid bound to plasma proteins, particularly albumin, ranges between ~50% to 64%. The volume of distribution of L-5-MTHF is estimated to be 32.0 L. Tetrahydrofolic acid derivatives are distributed to all body tissues but are stored primarily in the liver. Cerebrospinal fluid levels of folic acid are several times greater than serum levels of the drug.

Metabolism — The first step in the metabolism of folic acid is its reduction to dihydrofolate via dihydrofolate reductase. Subsequently, dihydrofolate is further reduced to tetrahydrofolate (THF). THF is further converted to methylene-THF by serine-hydroxymethyltransferase and reduced to physiologically active L-5-MTHF via methylenetetrahydrofolate reductase (MTHFR).

Elimination — After intravenous administration, folic acid is rapidly cleared from the plasma. Following oral administration, majority of the dose was recovered in the urine. A majority of the metabolic products appeared in the urine after 6 hours; excretion was generally complete within 24 hours. Small amounts of orally administered folic acid have also been recovered in the feces.

Simeticone is a chemically inert defoaming substance. It alters the interfaces of gas bubbles trapped in gastrointestinal mucus, helping bubbles break or combine so that gas can be expelled more easily.

The cited oral reference states that activated dimeticone is not absorbed from the gastrointestinal tract and is excreted unchanged in feces. Its local physical action therefore does not call for an invented systemic bioavailability, plasma peak or elimination half-life.

Pyridoxal phosphate and pyridoxamine phosphate are active vitamin B6 coenzymes involved in amino-acid metabolism. B6 also contributes to neurotransmitter synthesis, glycogen metabolism and hemoglobin formation.

Vitamin B6 is absorbed in the jejunum. Phosphorylated forms are dephosphorylated before free B6 enters by passive diffusion. The NIH review describes similar absorption from foods and supplements; much of a large pharmacological dose is rapidly eliminated in urine. This physiology does not supply a measured half-life for this formulation.

Niacin supplies precursors for NAD and NADP. These coenzymes participate in cellular oxidation-reduction reactions, energy metabolism and biosynthetic processes. This nutrient role should not be confused with evidence for a lipid-lowering effect of every niacin form.

Ingested niacin is absorbed mainly in the small intestine, with some stomach absorption. Tissues convert physiological amounts to NAD. Excess is metabolized in the liver to methylated and oxidized products that are eliminated in urine; very high intake can also produce urinary excretion of unchanged nicotinic acid or nicotinamide.

Riboflavin forms the coenzymes FMN and FAD, which participate in energy production and the metabolism of fats, drugs and steroids. These cofactors also contribute to the metabolic activation or conversion of other B vitamins.

Most riboflavin is absorbed in the proximal small intestine. The NIH fact sheet describes limited additional absorption from a single dose above approximately 27 mg and only small stores in liver, heart and kidneys. This is a nutrient-level absorption description, not a formulation-specific plasma concentration study.

Thiamine diphosphate is the principal active coenzyme form. It serves as a cofactor for enzymes in carbohydrate, amino-acid and lipid metabolism, supporting cellular energy metabolism.

Thiamine is absorbed in the small intestine by active transport at nutritional doses and passive diffusion at pharmacological doses. Dietary phosphorylated forms are hydrolyzed before absorption. Body stores, mainly in the liver, are small and turnover is rapid. These data concern thiamine and must not be substituted for the kinetics of benfotiamine.