Phylloquinone is often called vitamin K1 or phytonadione. It is a fat-soluble vitamin that is stable to air and moisture but decomposes in sunlight. It is found naturally in a wide variety of green plants. Phylloquinone is also an antidote for coumatetralyl. Vitamin K is needed for the posttranslational modification of certain proteins, mostly required for blood coagulation. MEPHYTON (Phytonadione tablets) are indicated in the following coagulation disorders which are due to faulty formation of factors II, VII, IX and X when caused by vitamin K deficiency or interference with vitamin K activity: anticoagulant-induced prothrombin deficiency caused by coumarin or indanedione derivatives; hypoprothrombinemia secondary to antibacterial therapy; hypoprothrombinemia secondary to administration of salicylates; hypoprothrombinemia secondary to obstructive jaundice or biliary fistulas but only if bile salts are administered concurrently, since otherwise the oral vitamin K will not be absorbed. MEPHYTON tablets possess the same type and degree of activity as does naturally-occurring vitamin K, which is necessary for the production via the liver of active prothrombin (factor II), proconvertin (factor VII), plasma thromboplastin component (factor IX), and Stuart factor (factor X). The prothrombin test is sensitive to the levels of three of these four factors II, VII, and X. Vitamin K is an essential cofactor for the gamma-carboxylase enzymes, which catalyze the posttranslational gamma-carboxylation of glutamic acid residues in inactive hepatic precursors of coagulation factors II (prothrombin), VII, IX, and X. Gamma-carboxylation converts these inactive precursors into active coagulation factors, which are secreted by hepatocytes into the blood. Supplementing with Phylloquinone results in a relief of vitamin K deficiency symptoms, which include easy bruisability, epistaxis, gastrointestinal bleeding, menorrhagia and hematuria. Oral phytonadione is adequately absorbed from the gastrointestinal tract only if bile salts are present. After absorption, phytonadione is initially concentrated in the liver, but the concentration declines rapidly. Very little vitamin K accumulates in tissues. Little is known about the metabolic fate of vitamin K. Almost no free unmetabolized vitamin K appears in bile or urine. In normal animals and humans, phytonadione is virtually devoid of pharmacodynamic activity. However, in animals and humans deficient in vitamin K, the pharmacological action of vitamin K is related to its normal physiological function; that is, to promote the hepatic biosynthesis of vitamin K-dependent clotting factors. MEPHYTON tablets generally exert their effect within 6 to 10 hours.

It is known that Vitamin E, traditionally known as α¬ tocopherol, is a mixture of eight different compounds, four tocopherols and four tocotrienols, each one being designated as α, β, γ and δ forms. The two groups differ in the hydrophobic tridecyl side chain which is saturated (phytyl) in tocopherols and unsaturated having three double bonds (geranyl) in tocotrienols. During the last few years, it has been found that all the eight forms are biologically active and perform specific functions. Clinical research has shown that mixture of tocotrienols and tocopherols offer synergistic protective action against heart ailments and cancer that is not exclusively offered by α¬tocopherol. The other advantage of mixed tocopherols and tocotrienols is their role in slowing down aging. Diseases like diabetes 1 and 2, autoimmune diseases, bacterial and viral infections, Alzheimer disease, fungal (Candida) infections are prevented by these compounds. It helps in the maintenance of bones, muscles, eyes (vision), memory, sleep, lungs, infertility, skin and wrinkles. Although all forms of Vitamin E exhibit antioxidant activity, it is known that the antioxidant activity of vitamin E is not sufficient to explain the vitamin's biological activity. Vitamin E's anti-atherogenic activity involves the inhibition of the oxidation of LDL and the accumulation of oxLDL in the arterial wall. Vitamin E's antithrombotic and anticoagulant activities involves the downregulation of the expression of intracellular cell adhesion molecule(ICAM)-1 and vascular cell adhesion molecule(VCAM)-1 that lowers the adhesion of blood components to the endothelium. Its antioxidant effects explain the neuroprotective effects of vitamin E. The immunomodulatory effects of Vitamin E have been demonstrated in vitro, where alpha-tocopherol increases mitogenic response of T lymphocytes from aged mice. The mechanism of this response by vitamin E is not well understood, however it has been suggested that vitamin E itself may have mitogenic activity independent of its antioxidant activity. The mechanism of action of vitamin E's antiviral effects (primarily against HIV-1) involves its antioxidant activity. Vitamin E reduces oxidative stress, which is thought to contribute to HIV-1 pathogenesis, as well as to the pathogenesis of other viral infections. Vitamin E also affects membrane integrity and fluidity and, since HIV-1 is a membraned virus, altering membrane fluidity of HIV-1 may interfere with its ability to bind to cell-receptor sites, thus decreasing its infectivity.

Secretin is a peptide hormone produced by S-cells of the small intestinal mucosa and involved in the regulation of pancreatic secretory activity. S-cells that are located in the mucous membrane of the duodenum and in the proximal part of the jejunum secrete the polypeptide prosecretin, an inactive precursor of secretin, which turns into secretin by the action of hydrochloric acid of the gastric juice. Being absorbed into the blood, secretin reaches the pancreas and pancreatic centroacinar cells have secretin receptors in their plasma membrane. As secretin binds to these receptors, it enhances the secretion of bicarbonate-rich fluid that flows into the intestine. Bicarbonate is a base that neutralizes the acid, thus establishing a pH favorable to the action of other digestive enzymes in the small intestine. Secretin also increases water and bicarbonate secretion from duodenal Brunner's glands to buffer the incoming protons of the acidic chyme and also reduces acid secretion by parietal cells of the stomach. Secretin is used in a diagnostic test for pancreatic function.

Tocopherol (alpha tocopheryl nicotinate) is an ester of tocopherol and nicotinic acid. Vitamin E (Tocopherol) is sold commercially as the esterified form (alpha tocopheryl acetate, alpha tocopheryl succinate and alpha tocopheryl nicotinate). Alpha tocopheryl nicotinate has antioxidant and vasodilatory properties. It can be used as a mild warming agent, without producing the redness typical for nicotinic acid. Tocopherol (alpha tocopheryl nicotinate) has been available in Japan since 1967. Tocopherol under the brand name Juvela N is approved in Japan for the treatment of symptoms accompanying hypertension, hyperlipidemia, peripheral circulatory disturbance resulting from arteriosclerosis obliterans. Tocopherol has being shown to inhibit platelet aggregation.

Angiotensin is a peptide hormone that causes vasoconstriction and a subsequent increase in blood pressure. It is part of the renin-angiotensin system, which is a major target for drugs that lower blood pressure. Angiotensin also stimulates the release of aldosterone, another hormone, from the adrenal cortex. Aldosterone promotes sodium retention in the distal nephron, in the kidney, which also drives blood pressure up. Angiotensin is an oligopeptide and is a hormone and a powerful dipsogen. Angiotensin I is derived from the precursor molecule angiotensinogen, a serum globulin produced in the liver. Angiotensin I is converted to angiotensin II (AII) through removal of two C-terminal residues by the enzyme angiotensin-converting enzyme (ACE), primarily through ACE within the lung (but also present in endothelial cells and kidney epithelial cells). ACE found in other tissues of the body has no physiological role (ACE has a high density in the lung, but activation here promotes no vasoconstriction, angiotensin II is below physiological levels of action). Angiotensin II acts as an endocrine, autocrine/paracrine, and intracrine hormone. Angiotensin II has prothrombotic potential through adhesion and aggregation of platelets and stimulation of PAI-1 and PAI-2. When cardiac cell growth is stimulated, a local (autocrine-paracrine) renin-angiotensin system is activated in the cardiac myocyte, which stimulates cardiac cell growth through protein kinase C. The same system can be activated in smooth muscle cells in conditions of hypertension, atherosclerosis, or endothelial damage. Angiotensin II is the most important Gq stimulator of the heart during hypertrophy, compared to endothelin-1 and α1 adrenoreceptors. Angiotensin II increases thirst sensation (dipsogen) through the subfornical organ of the brain, decreases the response of the baroreceptor reflex, and increases the desire for salt. It increases secretion of ADH in the posterior pituitary and secretion of ACTH in the anterior pituitary. It also potentiates the release of norepinephrine by direct action on postganglionic sympathetic fibers. Angiotensin II acts on the adrenal cortex, causing it to release aldosterone, a hormone that causes the kidneys to retain sodium and lose potassium. Elevated plasma angiotensin II levels are responsible for the elevated aldosterone levels present during the luteal phase of the menstrual cycle. Angiotensin II has a direct effect on the proximal tubules to increase Na+ reabsorption. It has a complex and variable effect on glomerular filtration and renal blood flow depending on the setting. Increases in systemic blood pressure will maintain renal perfusion pressure; however, constriction of the afferent and efferent glomerular arterioles will tend to restrict renal blood flow. The effect on the efferent arteriolar resistance is, however, markedly greater, in part due to its smaller basal diameter; this tends to increase glomerular capillary hydrostatic pressure and maintain glomerular filtration rate. A number of other mechanisms can affect renal blood flow and GFR. High concentrations of Angiotensin II can constrict the glomerular mesangium, reducing the area for glomerular filtration. Angiotensin II is a sensitizer to tubuloglomerular feedback, preventing an excessive rise in GFR. Angiotensin II causes the local release of prostaglandins, which, in turn, antagonize renal vasoconstriction. The net effect of these competing mechanisms on glomerular filtration will vary with the physiological and pharmacological environment. Angiotensin was independently isolated in Indianapolis and Argentina in the late 1930s (as 'angiotonin' and 'hypertensin', respectively) and subsequently characterised and synthesized by groups at the Cleveland Clinic and Ciba laboratories in Basel, Switzerland.