Rinavit syrup

Mechanism of action

Cyanocobalamin serves as a cofactor for methionine synthase and L-methylmalonyl-CoA mutase enzymes. Methionine synthase is essential for the synthesis of purines and pyrimidines that form DNA. L-methylmalonyl-CoA mutase is involved in the degradation of propionate, crucial for fat and protein metabolism. The lack of vitamin B12 results in the accumulation of methylmalonyl CoA, contributing to neurological manifestations. Additionally, it is vital for the synthesis of methionine from homocysteine, and its deficiency can lead to functional folate deficiency, which impacts red blood cell formation.

Pharmacodynamics

Cyanocobalamin corrects vitamin B12 deficiency and alleviates symptoms and laboratory abnormalities associated with pernicious anemia, such as megaloblastic indices, gastrointestinal lesions, and neurological damage. It is essential for growth, cell reproduction, hematopoiesis, nucleoprotein, and myelin synthesis. The drug significantly impacts fat and carbohydrate metabolism, as well as protein synthesis. Rapidly dividing cells, such as those in the bone marrow, have a high demand for vitamin B12. Parenteral administration of cyanocobalamin can quickly reverse the anemia and gastrointestinal symptoms of vitamin B12 deficiency, while also preventing the progression of related neurological damage.

Pharmacokinetics

Cyanocobalamin is absorbed in the intestine, primarily in the ileum, via specific transport mechanisms that may be impaired in individuals with intrinsic factor deficiency (as seen in pernicious anemia). Once absorbed, it is widely distributed in body tissues, with significant concentrations found in the liver, kidneys, and heart. The vitamin is stored in the liver, where it can be released into circulation as needed. Cyanocobalamin undergoes conversion to its active forms, methylcobalamin and adenosylcobalamin, which are utilized in various metabolic processes. The elimination half-life is variable, but it is generally excreted via urine as metabolites

Adverse effects

• Abdominal distension
• Decreased appetite
• Flatulence
• Nausea

Interactions

• Folic acid may interact with cyanocobalamin, especially in cases of megaloblastic anemia caused by folate deficiency.

Precautions

• Should not be given alone for pernicious anemia.
• Use caution in patients with Leber's disease, as it may worsen optic atrophy.

Pregnancy

Cyanocobalamin is essential during pregnancy as it helps prevent neural tube defects. It is advised that females of childbearing potential take 5 mg of folic acid daily before conception and throughout pregnancy.

Breast-feeding

Cyanocobalamin is generally considered safe during breastfeeding, but it is advised to monitor the infant for any adverse effects.

Storage

Store in a cool, dry place, away from direct sunlight. Protect from moisture.

Formulations

• Tablet: 1000 micrograms
• Tablet: 500 micrograms
• Tablet: 100 micrograms
• Oral solution: 50 micrograms per ml
• Solution for injection: 1000 micrograms per ml

Indications

• Papulopustular rosacea
• Inflammatory acne vulgaris

Dosage

Children: Refer to the BNF for Children for specific dosing recommendations.

Adults: For papulopustular rosacea, apply daily for up to 4 months. The treatment course may be repeated; discontinue if no improvement is observed after 3 months. For inflammatory acne vulgaris, apply twice daily, reduced to once daily or alternate days if irritation occurs.

Mechanism of action

Nicotinamide exhibits anti-inflammatory effects by inhibiting the release of pro-inflammatory cytokines and enhancing the barrier function of the skin. It is also involved in the NAD salvage pathway, which is essential for maintaining cellular energy levels and promoting cell repair mechanisms. Additionally, nicotinamide contributes to the synthesis of coenzymes involved in metabolic processes, including the conversion of niacin into NAD+.

Pharmacodynamics

Nicotinamide is known for its ability to improve skin hydration and reduce transepidermal water loss. It has been shown to decrease the appearance of acne lesions and rosacea by modulating inflammatory responses and accelerating cell turnover. Its antioxidant properties also help to protect the skin from oxidative stress and UV damage.

Pharmacokinetics

When applied topically, nicotinamide is absorbed through the skin layers, with minimal systemic absorption. Its peak plasma concentrations are generally low, and the drug has a half-life that varies depending on the route of administration. The metabolism of nicotinamide occurs primarily in the liver, where it is converted into its active forms, including NAD+. The elimination route is via the kidneys, with metabolites excreted in urine.

Contra-indications

• Pregnancy
• Severe acne involving large areas
• Severe skin reactions

Adverse effects

• Sunburn
• Skin reactions (common or very common)
• Cheilitis
• Eyelid oedema
• Flushing
• Dry skin
• Eye irritation
• Photosensitivity reactions
• Transient skin pigmentation changes

Interactions

• Clindamycin
• Topical retinoids
• Abrasive cleaners
• Comedogenic cosmetics

Precautions

• Avoid exposure to UV light, including sunlight and sunlamps
• Wash hands immediately after use
• Avoid contact with eyes and mucous membranes
• Use moisturizers to reduce the risk of skin irritation
• Discontinue treatment if severe irritation occurs

Pregnancy

Avoid use during pregnancy due to potential risks, as limited information is available regarding toxicity.

Breast-feeding

Amount of drug in milk after topical application is probably too small to be harmful; ensure infant does not come in contact with treated areas.

Storage

Store at room temperature away from moisture and light.

Formulations

• Cream
• Gel

Indications

• Vitamin C deficiency
• Scurvy
• Adjunct therapy in iron overload conditions

Dosage

Children: Child 1 month–3 years: 125–250 mg daily in 1–2 divided doses; Child 4–11 years: 250–500 mg daily in 1–2 divided doses; Child 12–17 years: 0.5–1 g daily in 1–2 divided doses.

Adults: 500 mg daily, taken in 1-2 divided doses, depending on the clinical condition and dietary needs.

Mechanism of action

Ascorbic acid functions primarily as a reducing agent, facilitating enzymatic reactions in the body, including the hydroxylation of proline and lysine in collagen synthesis. It also plays a role in the absorption of iron from the gastrointestinal tract and enhances the immune response.

Pharmacodynamics

Ascorbic acid is crucial for the maintenance of connective tissue and is involved in the metabolism of several amino acids. Its antioxidant properties help to mitigate oxidative stress and may play a role in reducing the risk of chronic diseases.

Pharmacokinetics

Ascorbic acid is absorbed in the intestines and is widely distributed throughout the body. The renal clearance of ascorbic acid is dose-dependent, with higher doses leading to increased excretion. The half-life varies but is generally around 15 to 30 minutes in healthy individuals, with tissue saturation levels influencing its retention.

Contra-indications

• Hypercalcaemia
• Hyperoxaluria
• Patients with cardiac dysfunction

Adverse effects

• Abdominal pain
• Headache
• Nausea
• Vomiting
• Diarrhoea
• Constipation
• Weight loss
• Polyuria
• Sweating
• Thirst
• Vertigo

Interactions

• Increases risk of cardiovascular adverse effects with iron chelators
• Increases risk of cardiovascular adverse effects with deferiprone
• Increases risk of cardiovascular adverse effects with desferrioxamine

Precautions

• Use with caution in patients with iron overload
• Monitor for symptoms of overdose

Pregnancy

High doses teratogenic in animals but therapeutic doses unlikely to be harmful.

Storage

Store in a cool, dry place away from direct sunlight.

Formulations

• Ascorbic acid 50 mg tablets
• Ascorbic acid 100 mg tablets
• Ascorbic acid 200 mg tablets
• Ascorbic acid 250 mg tablets
• Ascorbic acid 500 mg capsules

Indications

• Cancer (various types)
• Rheumatoid arthritis
• Multiple sclerosis
• Inflammatory bowel disease
• Psoriasis
• Hypercholesterolemia
• Infectious diseases (e.g., COVID-19)

Dosage

Children: Refer to the BNF for Children for paediatric dosing information, as it varies based on the specific monoclonal antibody and the condition being treated.

Adults: Refer to the specific monoclonal antibody product information for adult dosage, as it varies based on indication and specific agent used.

Mechanism of action

Monoclonal antibodies work by binding to specific proteins on the surface of cells. This binding can block the activity of certain proteins, mark cells for destruction by the immune system, or deliver cytotoxic agents directly to target cells. The mechanism of action varies depending on the specific monoclonal antibody but often involves modulation of immune response, inhibition of cell proliferation, and induction of apoptotic pathways.

Pharmacodynamics

The pharmacodynamics of monoclonal antibodies is primarily characterized by their specificity and affinity for targeted antigens. This leads to a variety of effects, including neutralization of pathogens, blockade of receptor-ligand interactions, and antibody-dependent cellular cytotoxicity. The clinical effects depend on the disease being treated and the specific antibody's action, such as inducing tumor regression in cancer or reducing inflammation in autoimmune diseases.

Pharmacokinetics

Monoclonal antibodies typically have a long half-life, allowing for less frequent dosing. They are generally administered intravenously or subcutaneously, with absorption and distribution influenced by the antibody's size and charge. The elimination occurs primarily through proteolytic degradation and intracellular recycling. Factors such as patient-specific variables, including immunogenicity and the presence of antibodies against the monoclonal antibody, can impact pharmacokinetics.

Interactions

• abatacept+monoclonalantibodies: Severe (increases risk of generalised infection (possibly life-threatening))
• anakinra+monoclonalantibodies: Severe (increases risk of generalised infection (possibly life-threatening))
• anthracyclines+monoclonalantibodies: Severe (increases risk of cardiotoxicity)
• filgotinib+monoclonalantibodies: Severe (increases risk of immunosuppression)
• monoclonalantibodies+fingolimod: Severe (increases risk of generalised infection (possibly life-threatening))
• normal immunoglobulin+monoclonalantibodies: Severe (affects effects)
• monoclonalantibodies+ozanimod: Severe (increases risk of generalised infection (possibly life-threatening))
• monoclonalantibodies+siponimod: Severe (increases risk of generalised infection (possibly life-threatening))
• monoclonalantibodies+vemurafenib: Severe (increases risk of hepatotoxicity)
• monoclonalantibodies+aminophylline: Moderate (decreases exposure)

Indications

• Angina pectoris
• Chronic stable angina
• Angina due to coronary artery disease

Dosage

Children: Refer to the appropriate prescribing guidelines and consult clinical references for paediatric dosing recommendations.

Adults: Refer to the appropriate prescribing guidelines and consult clinical references for specific adult dosing recommendations.

Mechanism of action

Isosorbide mononitrate is converted to nitric oxide (NO) in the body, which activates guanylate cyclase. This leads to an increase in cyclic guanosine monophosphate (cGMP) levels in smooth muscle cells, resulting in smooth muscle relaxation and vasodilation. This vasodilatory effect decreases preload and afterload on the heart, reducing myocardial oxygen demand and relieving symptoms of angina.

Pharmacodynamics

Mononitrate demonstrates a dose-dependent reduction in myocardial oxygen consumption by decreasing both venous return (preload) and systemic vascular resistance (afterload). It also facilitates coronary artery dilation, improving blood flow to ischemic myocardial tissue. The onset of action can be within 30 minutes, with peak effects generally occurring 1-2 hours after administration. The effects can last for 6-8 hours, depending on the dosing schedule.

Pharmacokinetics

Isosorbide mononitrate is well absorbed from the gastrointestinal tract, with a bioavailability of approximately 100% due to its oral formulation. It undergoes minimal first-pass metabolism. The peak plasma concentration is reached within 1-2 hours post-ingestion. The drug has a half-life of approximately 5 hours, and it is primarily eliminated via the kidneys as unchanged drug and metabolites. Steady-state concentrations are typically achieved within 24 hours of regular dosing.

Contra-indications

• Hypersensitivity to mononitrate or any of its components
• Severe hypotension
• Cardiogenic shock
• Severe anemia
• Concurrent use with phosphodiesterase inhibitors (e.g. sildenafil) due to risk of severe hypotension

Adverse effects

• Headache
• Dizziness
• Hypotension
• Flushing
• Tachycardia
• Palpitations
• Nausea
• Vomiting

Interactions

• Nitrates may enhance the effects of other antihypertensive agents
• Use with caution with alcohol, as it may exacerbate hypotensive effects
• Interactions may occur with phosphodiesterase type 5 inhibitors (e.g. sildenafil) leading to severe hypotension

Precautions

• Caution in patients with recent myocardial infarction or congestive heart failure
• Use with caution in patients with hepatic or renal impairment
• Monitor blood pressure regularly during treatment
• Consider tolerance development with long-term use

Pregnancy

Limited data available on the use of mononitrate in pregnancy. It should only be used if clearly needed and the benefits outweigh the risks.

Breast-feeding

Limited data available. Consider the benefits of breastfeeding against the need for the medication.

Storage

Store at room temperature, away from moisture and heat. Keep out of reach of children.

Formulations

• Extended-release tablets
• Sustained-release capsules
• Oral tablets

Indications

• Riboflavin deficiency
• Migraine prevention
• Cataract prevention
• General health maintenance

Dosage

Children: Refer to the BNF for Children for specific paediatric dosing recommendations.

Adults: Refer to the BNF for specific dosing recommendations for adults.

Mechanism of action

Riboflavin binds to riboflavin hydrogenase, riboflavin kinase, and riboflavin synthase. It is converted into two coenzymes: flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), which are essential for various oxidative enzyme systems, facilitating hydrogen transport. The antioxidant activity of riboflavin is largely due to its role as a precursor of FAD, which is involved in producing reduced glutathione, a major antioxidant enzyme cofactor.

Pharmacodynamics

Riboflavin is easily absorbed and plays a key role in numerous physiological functions, including energy production, red blood cell formation, and growth regulation. It is vital for the maintenance of healthy skin and eyes and has a role in the prevention and treatment of eye disorders, including cataracts. Riboflavin also supports thyroid activity and general health.

Pharmacokinetics

Riboflavin is readily absorbed in the gastrointestinal tract and is distributed throughout the body. It is primarily excreted in urine, with excess amounts eliminated, as riboflavin is a water-soluble vitamin. The pharmacokinetics of riboflavin can vary based on dietary intake and individual physiological conditions.

Adverse effects

• No significant adverse effects reported with normal dietary intake
• High doses may lead to yellow-orange discoloration of urine
• Rarely, hypersensitivity reactions

Precautions

• Use with caution in patients with known hypersensitivity to riboflavin or any of its components
• Consult healthcare provider before starting high-dose riboflavin supplements

Pregnancy

Riboflavin is generally considered safe during pregnancy and is important for fetal development. Adequate intake is necessary to prevent deficiency.

Breast-feeding

Riboflavin is excreted in breast milk, and adequate maternal intake is important for infant health.

Storage

Store in a tightly closed container at room temperature, away from light and moisture.

Formulations

• Tablets
• Capsules
• Oral solutions
• Powder for reconstitution

Dosage

Children: Refer to specific drug guidelines as dosing in units varies based on the drug and its clinical application.

Adults: Refer to specific drug guidelines as dosing in units varies based on the drug and its clinical application.

Mechanism of action

The mechanism of action of drugs measured in units depends on the specific substance. For example, insulin (measured in units) facilitates glucose uptake in cells by binding to insulin receptors, activating a signaling pathway that enhances glucose transporter translocation to the cell membrane. This results in a decrease in blood glucose levels. Similarly, other drugs measured in units may exert their effects through receptor binding, enzyme catalysis, or other biochemical interactions.

Pharmacodynamics

Pharmacodynamics describes the effects of the drug on the body and includes the relationship between drug concentration and effect. For substances measured in units, the pharmacodynamic response may be variable and is often dependent on the individual’s sensitivity to the drug, receptor availability, and other pharmacological factors. For instance, the effect of 1 unit of insulin can vary significantly among individuals based on their insulin sensitivity and metabolic state.

Pharmacokinetics

Pharmacokinetics refers to the absorption, distribution, metabolism, and excretion of drugs. For substances measured in units, the pharmacokinetic profile can differ widely. For instance, insulin is rapidly absorbed when administered subcutaneously, distributed throughout the body, metabolized by the liver and kidneys, and its effects can be observed within minutes. Other drugs may have different absorption rates, half-lives, and routes of elimination.

Pregnancy

Consult a healthcare professional. The safety of this drug during pregnancy has not been established.

Breast-feeding

Consult a healthcare professional. The safety of this drug during breastfeeding has not been established.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Indications

• Vitamin deficiency syndromes (e.g., scurvy for vitamin C deficiency, rickets for vitamin D deficiency)
• Support for immune function
• Antioxidant support
• Bone health maintenance
• Vision health
• Energy metabolism support

Dosage

Children: Refer to the BNF for Children for specific vitamin dosing guidelines, which depend on age and nutritional requirements.

Adults: Refer to specific vitamin guidelines as dosage varies significantly depending on the type of vitamin and individual needs.

Mechanism of action

Vitamins function primarily as coenzymes or precursors for coenzymes in enzymatic reactions. For instance, B vitamins are involved in energy metabolism, while vitamins A, C, D, E, and K support various physiological functions including vision, antioxidant activity, calcium regulation, and blood clotting. Each vitamin has a unique mechanism of action based on its structure and role in the body.

Pharmacodynamics

Vitamins exert their effects at the cellular level, influencing metabolic pathways, gene expression, and immune responses. For example, vitamin D regulates calcium and phosphate homeostasis, while vitamin A is crucial for vision and immune function. Deficiencies in vitamins can lead to a range of disorders, highlighting their importance in maintaining health.

Pharmacokinetics

The pharmacokinetics of vitamins vary widely. Fat-soluble vitamins (A, D, E, and K) are stored in liver and adipose tissues and can be released into circulation as needed. Water-soluble vitamins (B-complex and C) are not stored and must be consumed regularly, with excess amounts excreted in urine. Absorption rates, half-lives, and distribution can also differ based on the specific vitamin and individual metabolic factors.

Interactions

• tretinoin+vitamin: Severe (increases risk of vitamin toxicity)
• retinoids+vitamin: Severe (increases risk of vitamin toxicity)
• retinoids+vitamin: Moderate (increases risk of toxicity)
• carbamazepine+vitamin: Unknown (decreases effects)
• cobicistat+vitamin: Unknown (increases exposure)
• vitamin D substances+digoxin: Unknown (increases risk of toxicity)
• idelalisib+vitamin: Unknown (increases exposure)
• clarithromycin+vitamin: Unknown (increases exposure)

Pregnancy

Consult healthcare professional before use. Vitamin supplementation during pregnancy should be carefully managed to avoid hypervitaminosis.

Breast-feeding

Consult healthcare professional before use. Some vitamins can pass into breast milk and may affect the infant.

Storage

Store in a cool, dry place, away from direct sunlight. Ensure it is kept out of reach of children.

Formulations

• {'name': 'Vitamin A', 'form': 'Capsule', 'strength': '10000 IU'}
• {'name': 'Vitamin D', 'form': 'Tablet', 'strength': '1000 IU'}
• {'name': 'Vitamin E', 'form': 'Softgel', 'strength': '400 IU'}

Mechanism of action

Vitamin B12 serves as a cofactor for _methionine synthase_ and _L-methylmalonyl-CoA mutase_ enzymes. Methionine synthase is essential for the synthesis of purines and pyrimidines that form DNA. L-methylmalonyl-CoA mutase converts L-methylmalonyl-CoA to _succinyl-CoA_ in the degradation of propionate, an important reaction required for both fat and protein metabolism. It is a lack of vitamin B12 cofactor in the above reaction and the resulting accumulation of methylmalonyl CoA that is believed to be responsible for the neurological manifestations of B12 deficiency. Succinyl-CoA is also necessary for the synthesis of hemoglobin. In tissues, vitamin B12 is required for the synthesis of _methionine_ from homocysteine. Methionine is required for the formation of S-adenosylmethionine, a methyl donor for nearly 100 substrates, comprised of DNA, RNA, hormones, proteins, as well as lipids. Without vitamin B12, tetrahydrofolate cannot be regenerated from 5-methyltetrahydrofolate, and this can lead to functional folate deficiency,. This reaction is dependent on methylcobalamin (vitamin B12) as a co-factor and is also dependent on folate, in which the methyl group of methyltetrahydrofolate is transferred to homocysteine to form _methionine_ and _tetrahydrofolate_. Vitamin B12 incorporates into circulating folic acid into growing red blood cells; retaining the folate in these cells. A deficiency of vitamin B12 and the interruption of this reaction leads to the development of megaloblastic anemia.

Pharmacodynamics

**General effects** Cyanocobalamin corrects vitamin B12 deficiency and improves the symptoms and laboratory abnormalities associated with pernicious anemia (megaloblastic indices, gastrointestinal lesions, and neurologic damage). This drug aids in growth, cell reproduction, hematopoiesis, nucleoprotein, and myelin synthesis. It also plays an important role in fat metabolism, carbohydrate metabolism, as well as protein synthesis. Cells that undergo rapid division (for example, epithelial cells, bone marrow, and myeloid cells) have a high demand for vitamin B12. **Parenteral cyanocobalamin effects** The parenteral administration of vitamin B12 rapidly and completely reverses the megaloblastic anemia and gastrointestinal symptoms of vitamin B12 deficiency. Rapid parenteral administration of vitamin B12 in deficiency related neurological damage prevents the progression of this condition. **Nasal spray effects** In 24 vitamin B12 deficient patients who were already stabilized on intramuscular (IM) vitamin B12 therapy, single daily doses of intranasal cyanocobalamin for 8 weeks lead to serum vitamin B12 concentrations that were within the target therapeutic range (>200 ng/L).

Mechanism of action

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. Riboflavin is converted to 2 coenzymes, flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), which are necessary for normal tissue respiration. Riboflavin is also required for activation of pyridoxine, conversion of tryptophan to niacin, and may be involved in maintaining erythrocyte integrity. Riboflavin functions as the coenzyme for flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN), which primarily influence hydrogen transport in oxidative enzyme systems (eg, cytochrome C reductase, succinic dehydrogenase, xanthine oxidase). Two active forms of riboflavin exist ... coenzyme flavin mononucleotide (FMN) and coenzyme flavin adenine dinucleotide (FAD). They are formed by reaction of riboflavin with 1 and 2 molecules of ATP as follow: riboflavin + ATP = riboflavin-P (FMN) + ADP; FMN + ATP = riboflavin-ADP (FAD) + PP. Riboflavin is a water-soluble, yellow, fluorescent compound. The primary form of the vitamin is as an integral component of the coenzymes flavin mononucleotide (FMN) and flavin-adenine dinucleotide (FAD). It is in these bound coenzyme forms that riboflavin functions as a catalyst for redox reactions in numerous metabolic pathways and in energy production. ... The redox reactions in which flavocoenzymes participate include flavoprotein-catalyzed dehydrogenations that are both pyridine nucleotide (niacin) dependent and independent, reactions with sulfur-containing compounds, hydroxylations, oxidative decarboxylations (involving thiamin as its pyrophosphate), dioxygenations, and reduction of oxygen to hydrogen peroxide. There are obligatory roles of flavocoenzymes in the formation of some vitamins and their coenzymes. For example, the biosynthesis of two niacin-containing coenzymes from tryptophan occurs via FAD-dependent kynurenine hydroxylase, an FMN-dependent oxidase catalyzes the conversion of the 5'-phosphates of vitamin B6 to coenzymic pyridoxal 5'-phosphate, and an FAD-dependent dehydrogenase reduces 5,10-methylene-tetrahydrofolate to the 5'-methyl product that interfaces with the B12-dependent formation of methionine from homocysteine and thus with sulfur amino acid metabolism. For more Mechanism of Action (Complete) data for Riboflavin (7 total), please visit the HSDB record page.

Pharmacodynamics

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.