VITAMAX CAPSULES

Indications

• Severe extensive psoriasis resistant to other forms of therapy
• Palmoplantar pustular psoriasis
• Severe congenital ichthyosis
• Severe Darier’s disease (keratosis follicularis)

Dosage

Children: Child 1 month–11 years: 0.5 mg/kg once daily; increased if necessary to 1 mg/kg once daily, maximum 35 mg per day. Child 12–17 years: Initially 25–30 mg daily for 2–4 weeks, then adjusted according to response to 25–50 mg daily, increased to up to 75 mg daily.

Adults: Initially 25–30 mg daily for 2–4 weeks, then adjusted according to response to 25–50 mg daily, increased to up to 75 mg daily if necessary.

Mechanism of action

Acitretin binds to retinoic acid receptors, influencing gene expression involved in cellular differentiation, proliferation, and apoptosis, thereby normalizing skin cell turnover and reducing inflammation.

Pharmacodynamics

Acitretin affects the differentiation and proliferation of epithelial cells, leading to normalization of keratinization and a reduction in the severity of skin conditions such as psoriasis.

Pharmacokinetics

Acitretin is rapidly absorbed after oral administration, with peak plasma concentrations occurring in 2 to 4 hours. It has a half-life of approximately 49 hours and is primarily metabolized in the liver. Its elimination is affected by food intake, with higher bioavailability when taken with food.

Contra-indications

• Pregnancy
• Severe liver disease
• Hyperlipidaemia
• Hypersensitivity to acitretin or any excipients

Adverse effects

• Abdominal pain
• Arthralgia
• Dizziness
• Nausea
• Oral disorders
• Peripheral oedema
• Skin reactions
• Thirst
• Vomiting
• Xerophthalmia
• Vision disorders
• Bone pain
• Exostosis
• Idiopathic intracranial hypertension
• Peripheral neuropathy
• Hearing impairment
• Hyperhidrosis
• Malaise
• Pyogenic granuloma
• Taste alteration
• Tinnitus

Interactions

• Severe interaction with methotrexate (increases concentration)
• Unknown interaction with alcohol (may increase concentration)

Precautions

• Monitor for signs of severe headache, nausea, vomiting, or visual disturbances
• Effective contraception required for females of child-bearing potential
• Avoid alcohol during treatment and for 2 months after stopping treatment

Pregnancy

Avoid-teratogenic.

Breast-feeding

Use is not recommended.

Storage

Store below 25°C. Protect from light.

Formulations

• Capsules: 10 mg, 25 mg, 30 mg
• Solution for injection: 10 mg/1 ml

Indications

• Management of photosensitivity reactions
• Erythropoietic protoporphyria

Dosage

Children: Child 1–4 years: 60–90 mg daily, Child 5–8 years: 90–120 mg daily, Child 9–11 years: 120–150 mg daily, to be given as a single dose or in divided doses.

Adults: Refer to the BNF for specific dosing guidelines.

Mechanism of action

Betacarotene acts as an antioxidant and a precursor to vitamin A, which plays a critical role in cellular function, vision, growth, immune function, and skin health.

Pharmacodynamics

As a provitamin, betacarotene is converted to retinol (vitamin A) in the body, supporting various biological functions, including the maintenance of epithelial tissues and the modulation of immune responses.

Pharmacokinetics

Betacarotene is absorbed from the gastrointestinal tract and is stored in the liver. Its absorption can be influenced by dietary fat intake. It is primarily metabolized in the liver and has a relatively long half-life due to its storage in fat tissues.

Pregnancy

Safety in pregnancy has not been established; use only if clearly needed.

Breast-feeding

Excretion in breast milk is unknown; use with caution.

Storage

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

Formulations

• Oral preparations containing beta-carotene

Indications

• Vitamin B2 deficiency
• Isoniazid-induced neuropathy (prophylaxis and treatment)
• Metabolic diseases
• Cystathioninuria
• Homocystinuria
• Wilson's disease
• Prevention of penicillamine-induced neuropathy

Mechanism of action

Riboflavin acts as a precursor to flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), which are essential coenzymes in various enzymatic reactions. It binds to riboflavin hydrogenase, riboflavin kinase, and riboflavin synthase, facilitating the production of FMN and FAD. These coenzymes are critical for normal tissue respiration and energy metabolism, influencing hydrogen transport in oxidative enzyme systems such as cytochrome C reductase and succinic dehydrogenase. Moreover, riboflavin contributes to the antioxidant activity by aiding in the production of reduced glutathione, a key antioxidant in the body.

Pharmacodynamics

Riboflavin is an easily absorbed, water-soluble micronutrient that supports energy production by assisting in the metabolism of fats, carbohydrates, and proteins. It is vital for red blood cell formation, antibody production, and regulating growth and reproduction. The vitamin plays a significant role in maintaining healthy skin, nails, and hair, as well as supporting thyroid activity. Riboflavin also has therapeutic implications in preventing or treating various eye disorders, including cataracts.

Pharmacokinetics

Riboflavin is rapidly absorbed in the gastrointestinal tract, with its bioavailability influenced by dietary intake. It is primarily excreted through urine, with excess intake leading to bright yellow urine, which is a harmless side effect. The vitamin does not accumulate in the body, necessitating regular dietary intake to maintain adequate levels.

Adverse effects

• Urine discolouration
• Peripheral neuritis

Precautions

• With intravenous use, risk of cardiovascular collapse; resuscitation facilities must be available and monitor closely.

Pregnancy

Crosses the placenta but no adverse effects reported; information at high doses limited.

Breast-feeding

Present in breast milk but no adverse effects reported; information at high doses limited.

Storage

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

Formulations

• 100 mg modified-release tablets
• 50 mg capsules
• 100 mg capsules
• 100 mg tablets
• Oral solution

Indications

• Selenium deficiency
• Supportive therapy in conditions requiring antioxidant support
• Potential adjunct in cancer prevention strategies

Dosage

Children: Refer to BNF for Children for specific dosing information.

Adults: Initially 100–500 micrograms daily, adjusted according to response and serum levels.

Mechanism of action

Selenium is metabolized to selenophosphate and selenocysteine, which are essential for the synthesis of selenoproteins. This process involves the incorporation of selenium into proteins through a specialized tRNA that recognizes the RNA sequence UGA, which is facilitated by SECIS structures and SBP-2 proteins. Key selenoproteins, like glutathione peroxidases, help protect cells from oxidative damage, thus playing a significant role in reducing the risk of diseases such as atherosclerosis and certain cancers.

Pharmacodynamics

Selenium is incorporated into various selenoproteins that perform essential functions, including antioxidant activity, redox balance, and regulation of thyroid hormones. Its role in antioxidant defense mechanisms is particularly important for protecting cells against reactive oxygen species (ROS). Selenium supplementation has been linked to improved immune function and potential cancer prevention.

Pharmacokinetics

Selenium is absorbed through the gastrointestinal tract, and its bioavailability can vary based on the source and form of selenium. Once absorbed, it is distributed to various tissues, where it is incorporated into selenoproteins. Selenium is primarily excreted through urine, and its half-life can depend on dietary intake and individual metabolism. Selenium status can be assessed through blood levels of selenoproteins and selenium itself.

Adverse effects

• Nausea
• Anaemia
• Aplastic anaemia
• Skin reactions
• Gastrointestinal disorders

Precautions

• Selenium supplementation should not be given unless there is good evidence of deficiency.
• Use caution in patients with a history of hypersensitivity to selenium or its compounds.

Pregnancy

Limited information is available regarding selenium supplementation during pregnancy. Consult specialist sources for guidance.

Breast-feeding

Limited information is available; the effect of selenium on copper levels in milk is conflicting, and its impact on the infant is unknown.

Storage

After opening, store in a refrigerator (2–8°C).

Formulations

• Tablets (e.g., L-Selenomethionine 200 micrograms, SelenoPrecise 100 micrograms)
• Capsules (e.g., Trientine dihydrochloride 250 mg)
• Injection solutions (e.g., Sodium selenite 50 micrograms per 1 ml)

Indications

• Vitamin D deficiency
• Rickets
• Osteomalacia
• Osteoporosis
• Hypoparathyroidism

Dosage

Adults: The usual adult dose for vitamin D deficiency is 800 to 2000 IU daily, depending on the severity of deficiency and clinical condition. Higher doses may be used under medical supervision.

Mechanism of action

Cholecalciferol is converted to its active forms, 25-hydroxyvitamin D in the liver and 1,25-dihydroxyvitamin D in the kidneys. These metabolites enhance the intestinal absorption of calcium and phosphorus, increase serum calcium levels, and mobilize these minerals from bone. This process is regulated by parathyroid hormone, which influences calcium and phosphate metabolism, particularly in the kidneys.

Pharmacodynamics

The pharmacodynamics of cholecalciferol involve its conversion to active metabolites that play a significant role in calcium and phosphorus homeostasis. The metabolites facilitate intestinal absorption of these minerals, promote bone mineralization, and influence renal reabsorption. The onset of action occurs within 10 to 24 hours following administration, as metabolic activation is required for its biological effects.

Pharmacokinetics

Cholecalciferol is absorbed in the gastrointestinal tract, and its absorption is enhanced by the presence of dietary fats. It is transported in the bloodstream bound to vitamin D-binding protein. Once in the liver, it undergoes hydroxylation to form 25-hydroxyvitamin D, which is further converted in the kidneys to the active form, 1,25-dihydroxyvitamin D. The elimination half-life of cholecalciferol varies, typically spanning several days, and it is primarily excreted in bile and urine.

Adverse effects

• Hypercalcemia
• Hypercalciuria
• Nausea
• Vomiting
• Constipation
• Weakness
• Fatigue

Interactions

• May enhance the effects of thiazide diuretics, leading to increased risk of hypercalcemia
• Anticonvulsants may increase metabolism of vitamin D, leading to reduced effectiveness
• Cholestyramine may reduce absorption of vitamin D

Precautions

• Monitor serum calcium levels in patients with renal impairment
• Caution in patients with a history of hypercalcemia or hyperparathyroidism
• Use with caution in patients taking other medications that affect calcium metabolism

Pregnancy

Cholecalciferol can be used during pregnancy if indicated, as vitamin D is essential for fetal bone development.

Breast-feeding

Cholecalciferol is excreted in breast milk, but is generally considered safe during breastfeeding.

Storage

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

Formulations

• Capsules
• Tablets
• Liquid formulations

Indications

• Biotin deficiency
• Dermatological conditions (e.g., hair loss, brittle nails)
• Metabolic disorders
• Supporting energy metabolism

Dosage

Children: Refer to specific pediatric guidelines for biotin doses, which are typically adjusted based on age and weight.

Adults: Refer to specific guidelines for biotin supplementation as doses vary based on condition and formulation.

Mechanism of action

Dbiotine functions as a coenzyme for carboxylase enzymes, facilitating the conversion of pyruvate to oxaloacetate, which is a crucial step in gluconeogenesis and citric acid cycle. It also aids in the synthesis of fatty acids and branched-chain amino acids by activating the relevant enzymes in metabolic pathways.

Pharmacodynamics

Dbiotine enhances the body's ability to metabolize carbohydrates, fats, and proteins. It plays a vital role in the regulation of energy metabolism and helps maintain healthy skin and hair. Its activity is essential for numerous enzymatic reactions that contribute to cellular function and energy production.

Pharmacokinetics

Dbiotine is well-absorbed from the gastrointestinal tract, with bioavailability generally being high. It is distributed widely throughout the body, particularly in the liver, kidneys, and brain. The elimination half-life of biotin is approximately 27 hours, and it is primarily excreted via the urine. Due to its water-soluble nature, excess amounts are readily excreted, minimizing the risk of toxicity.

Pregnancy

There is limited data on the safety of biotin during pregnancy. Consultation with a healthcare provider is recommended.

Breast-feeding

Biotin is considered safe during breastfeeding as it is a water-soluble vitamin. However, consultation with a healthcare provider is advised.

Storage

Store in a cool, dry place, away from light and moisture.

Indications

• Cognitive enhancement
• Memory improvement
• Mood stabilization
• Potential treatment of attention disorders

Dosage

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

Adults: Refer to BNF for specific dosing recommendations.

Mechanism of action

Deanol is believed to increase the levels of acetylcholine in the brain by serving as a precursor to the neurotransmitter. Acetylcholine is crucial for various cognitive functions, including memory and learning. It may also influence brain wave patterns and has been suggested to enhance synaptic transmission.

Pharmacodynamics

Deanol exhibits mild psychoactive effects, potentially improving mood and cognitive function. Its mechanism of action involves the modulation of neurotransmitter release, particularly acetylcholine, which plays a significant role in the central nervous system's functioning. The compound is thought to have a role in enhancing synaptic plasticity and neuroprotection.

Pharmacokinetics

The pharmacokinetic profile of deanol is not extensively characterized. However, it is generally understood that it is absorbed in the gastrointestinal tract following oral administration. The metabolism and excretion pathways are not well defined, and further research is needed to fully understand its bioavailability and half-life.

Pregnancy

There is insufficient data on the use of deanol in pregnancy. Caution is advised.

Breast-feeding

It is not known if deanol is excreted in human milk. Caution is recommended.

Storage

Store in a cool, dry place away from light.

Formulations

• {'formulation': 'Capsule', 'strength': 'various strengths available'}
• {'formulation': 'Liquid', 'strength': 'various concentrations available'}

Indications

• Calcium deficiency
• Osteoporosis prevention
• Osteomalacia
• Rickets
• Dietary supplementation in individuals with increased calcium and phosphorus requirements

Dosage

Children: Refer to established guidelines for specific dosing based on clinical indications and individual patient needs.

Adults: Refer to established guidelines for specific dosing based on clinical indications and individual patient needs.

Mechanism of action

Dicalcium phosphate dissociates in the gastrointestinal tract to release calcium and phosphate ions. Calcium plays a vital role in various physiological processes, including muscle contraction, neurotransmitter release, and blood coagulation. The phosphate ions are essential for energy metabolism and are integral to the formation of ATP (adenosine triphosphate), nucleic acids, and cellular membranes. The availability of these ions supports bone mineralization and overall skeletal integrity.

Pharmacodynamics

The pharmacodynamics of dicalcium phosphate involves its role in maintaining calcium and phosphate homeostasis in the body. Adequate levels of calcium are critical for normal bone metabolism, while phosphate is necessary for the formation of hydroxyapatite in bone tissue. The balance of these minerals is regulated by hormones such as parathyroid hormone and calcitriol, which modulate their absorption in the intestines and reabsorption in the kidneys. Supplementation with dicalcium phosphate can help alleviate deficiencies and support bone health.

Pharmacokinetics

Dicalcium phosphate is absorbed in the gastrointestinal tract, with varying absorption rates depending on the presence of other dietary components. Calcium absorption occurs primarily in the small intestine, while phosphate absorption can occur throughout the gastrointestinal tract. After absorption, calcium is distributed to bones, teeth, and soft tissues, while excess calcium is excreted through urine. The pharmacokinetics may be influenced by factors such as age, dietary habits, and the presence of gastrointestinal disorders.

Adverse effects

• Gastrointestinal disturbances (nausea, constipation)
• Hypercalcemia
• Kidney stones
• Fatigue
• Muscle weakness

Interactions

• May interact with calcium channel blockers
• Increased risk of hypercalcemia with thiazide diuretics
• May affect the absorption of certain antibiotics (e.g., tetracyclines)

Precautions

• Use with caution in patients with renal impairment
• Monitor calcium levels in patients receiving high doses
• Consider potential interactions with other medications

Pregnancy

Dicalcium is generally considered safe in pregnancy when used as directed, but high doses should be avoided.

Breast-feeding

Calcium is an essential nutrient during breastfeeding, but excessive supplementation should be approached with caution.

Storage

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

Formulations

• Tablets
• Powders
• Chewable tablets

Indications

• Severe psoriasis
• Disorders of keratinization

Dosage

Children: Refer to the BNF for Children for appropriate dosing guidelines in paediatric populations.

Adults: Refer to the BNF for specific dosing recommendations based on individual patient circumstances and condition severity.

Mechanism of action

The mechanism of action of etretinate's active metabolite, acitretin, is not fully understood. However, it is believed to target specific retinoid receptors in the skin, helping to normalize the growth cycle of skin cells.

Pharmacodynamics

The active metabolite of etretinate, acitretin, is a retinoid with a chemical structure similar to vitamin A. It plays a vital role in the normal growth of skin cells by inhibiting excessive cell growth and keratinisation, which is the thickening of skin cells due to protein deposition. This action reduces skin thickening, plaque formation, and scaling commonly seen in conditions such as psoriasis.

Pharmacokinetics

Etretinate is well absorbed from the gastrointestinal tract, with peak plasma concentrations occurring approximately 2 to 4 hours after oral administration. It is highly lipophilic, leading to a large volume of distribution. The drug is primarily metabolized in the liver to its active form, acitretin, and has a long half-life, necessitating caution in use, especially regarding potential accumulation and toxicity. It is excreted mainly in the urine.

Contra-indications

• Pregnancy
• Breastfeeding
• Hypervitaminosis A
• Severe hepatic impairment
• Severe renal impairment
• Concurrent use of tetracyclines

Adverse effects

• Dry skin
• Chapped lips
• Nasal dryness
• Pruritus
• Erythema
• Fatigue
• Headache
• Muscle pain
• Elevated liver enzymes
• Elevated triglycerides

Interactions

• Tetracyclines may increase the risk of intracranial hypertension
• Concomitant use with other retinoids can increase toxicity
• Alcohol may increase the risk of liver toxicity
• St. John's Wort may reduce the effectiveness of etretinate

Precautions

• Regular monitoring of liver function tests
• Avoiding excessive sun exposure due to increased photosensitivity
• Caution in patients with a history of depression
• Avoiding use in children unless deemed necessary

Pregnancy

Etretinate is contraindicated in pregnancy due to the risk of teratogenic effects.

Breast-feeding

Etretinate is contraindicated during breastfeeding as it may be excreted in breast milk.

Storage

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

Formulations

• Capsules

Indications

• Management of chronic pain
• Treatment of anxiety disorders
• Adjunct therapy for depression
• Control of seizures in certain types of epilepsy

Dosage

Children: Refer to the relevant pediatric dosing guidelines or specific clinical protocols for dosing instructions.

Adults: Refer to specific clinical guidelines or the product information for appropriate dosing recommendations.

Mechanism of action

The precise mechanism of action for Extrac is not well-documented in available literature. However, it is believed to interact with specific cellular pathways or receptors to elicit its therapeutic effects. Generally, medications in its class may work by modulating neurotransmitter levels, affecting ion channels, or influencing metabolic processes.

Pharmacodynamics

Pharmacodynamics of Extrac entails its effects on the body and the relationship between drug concentration and therapeutic effect. Typically, the efficacy and safety profile is determined by its dose-response curve, with specific attention to adverse effects and therapeutic windows. The drug may exhibit dose-dependent effects, necessitating careful monitoring during treatment.

Pharmacokinetics

Pharmacokinetics of Extrac involves absorption, distribution, metabolism, and excretion. It is usually absorbed after administration and distributed throughout the body, often reaching peak plasma concentrations within a specified timeframe. The metabolism may occur in the liver, and elimination is typically via renal or biliary pathways, with half-life varying based on individual patient factors.

Pregnancy

Consult with a healthcare provider before use, as safety in pregnancy has not been established.

Breast-feeding

Consult with a healthcare provider before use, as safety during breastfeeding has not been established.

Storage

Store at room temperature, away from direct sunlight and moisture.

Indications

• Fatigue
• Stress management
• Cognitive enhancement
• Immune support
• General well-being

Dosage

Children: Refer to specific product guidelines, as dosing in children should be determined by a healthcare professional.

Adults: Refer to specific product guidelines, as dosing can vary based on formulation and intended use.

Mechanism of action

Ginseng is thought to exert its effects through several mechanisms, including modulation of the hypothalamic-pituitary-adrenal (HPA) axis, enhancement of antioxidant activity, and regulation of neurotransmitter levels. Ginsenosides, the active compounds in ginseng, may influence cellular signaling pathways, promote neuroprotection, and enhance immune responses.

Pharmacodynamics

The pharmacodynamic effects of ginseng are attributed primarily to its active constituents, ginsenosides, which interact with various receptors and enzymes in the body. These interactions can lead to increased energy metabolism, improved cognitive function, enhanced physical performance, and modulation of the immune system. Ginseng may also exhibit adaptogenic properties, helping the body to maintain homeostasis under stress.

Pharmacokinetics

Ginsenosides undergo extensive metabolism in the body, primarily by the liver. Bioavailability can vary significantly based on the specific ginsenoside and the method of administration. Ginseng is usually administered orally, with effects typically observed within several hours after ingestion. The elimination half-life of ginsenosides can vary based on the specific compound and individual metabolism, with some studies suggesting that effects may persist for several hours to days.

Adverse effects

• Insomnia
• Headache
• Gastrointestinal disturbances
• Nervousness
• Hypertension
• Allergic reactions

Interactions

• May interact with anticoagulants (e.g., warfarin)
• May enhance the effects of caffeine
• May affect insulin levels and blood sugar control
• Potential interaction with immunosuppressants

Precautions

• Use with caution in patients with hypertension
• May cause sleep disturbances; avoid use before bedtime
• Should be used cautiously in patients with diabetes
• Consult a healthcare provider before use in individuals with autoimmune conditions

Pregnancy

Limited data available. Generally not recommended due to potential hormonal effects.

Breast-feeding

Limited data available. Consult a healthcare provider before use.

Storage

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

Formulations

• Dried root
• Powdered extract
• Capsules
• Tinctures
• Teas

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)

Mechanism of action

The biological activity of hydrogen chloride is primarily due to its high solubility in water. Upon dissolution, it dissociates to form hydronium ions, which act as proton donors, facilitating catalytic reactions with organic molecules. This capability may lead to cellular injury and necrosis.

Pharmacodynamics

As a strong acid, monohydrochloride can lower pH levels in biological systems, influencing numerous biochemical pathways. Its reactive nature allows it to interact with proteins, lipids, and nucleic acids, potentially leading to cellular damage and influencing metabolic processes.

Pharmacokinetics

Monohydrochloride is rapidly dissociated in aqueous environments, leading to immediate biological effects. The rapid formation of hydronium ions plays a crucial role in its pharmacokinetic profile, as these ions can affect local pH and influence the activity of various enzymes and cellular pathways. Specific absorption, distribution, metabolism, and excretion profiles are not detailed in the provided data.

Pregnancy

There is limited data on the use of monohydrochloride during pregnancy. Consult local guidelines and consider risk versus benefit.

Breast-feeding

Consult local guidelines regarding the use of monohydrochloride while breastfeeding, as data is limited.

Storage

Store in a cool, dry place, away from direct sunlight. Ensure it is kept in a tightly closed container.

Indications

• Allergic rhinitis (hay fever)
• Respiratory allergies
• Nutritional supplement for general health
• Potential anti-inflammatory treatment

Dosage

Children: Dosage varies based on the specific pollen product and indication. Refer to product-specific guidelines.

Adults: Dosage varies based on the specific pollen product and indication. Refer to product-specific guidelines.

Mechanism of action

Pollen's mechanism of action is not fully elucidated, but it is believed to exert effects through the modulation of immune responses. It may influence the activity of various immune cells, including mast cells and T lymphocytes, thereby affecting inflammatory pathways. Pollen may also contain flavonoids and phenolic compounds that contribute to its antioxidant effects, helping to neutralize free radicals and reduce oxidative stress.

Pharmacodynamics

Pollen exhibits several pharmacodynamic properties, including anti-inflammatory and immunomodulatory effects. It may help in reducing the severity of allergic reactions by influencing histamine release and modulating cytokine production. The antioxidant properties of pollen can also contribute to overall health by protecting cells from oxidative damage. However, its effects can vary significantly based on the source of the pollen and individual patient factors.

Pharmacokinetics

The pharmacokinetics of pollen can vary widely depending on its source and preparation. Generally, when consumed, pollen components are absorbed through the gastrointestinal tract. However, the specific absorption rates, distribution, metabolism, and excretion of pollen constituents are not well-studied. The bioavailability of active compounds may be affected by factors such as food interactions and individual metabolism.

Adverse effects

• Allergic reactions
• Respiratory irritation
• Skin rashes
• Anaphylaxis in sensitive individuals

Precautions

• Use with caution in individuals with known pollen allergies
• Monitor for respiratory symptoms in sensitive populations

Pregnancy

Limited data available on the safety of pollen exposure during pregnancy. Consult a healthcare provider for advice.

Breast-feeding

Limited data available on the safety of pollen exposure during breastfeeding. Consult a healthcare provider for advice.

Storage

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

Indications

• Anti-inflammatory effects
• Antioxidant support
• Immune system modulation
• Support in chronic diseases
• General wellness and health maintenance

Dosage

Children: Paediatric dosing for radix extracts should be approached with caution and is best determined by a healthcare provider, taking into account the child's age, weight, and health condition.

Adults: Dosage for radix extracts varies widely based on the specific herb and its intended use. It is advisable to refer to specific guidelines or consult with a healthcare professional for dosage recommendations.

Mechanism of action

The mechanisms of action for radix extracts are diverse and depend on the specific herb. Generally, these extracts may exert their effects through modulation of various signaling pathways, including the inhibition of pro-inflammatory cytokines, enhancement of antioxidant defenses, and regulation of immune cell activity. Many radix formulations contain bioactive compounds that interact with specific molecular targets, leading to physiological changes that contribute to their therapeutic effects.

Pharmacodynamics

Pharmacodynamics of radix extracts involves their interactions with biological systems. They may exhibit properties such as anti-inflammatory effects, reduction of oxidative stress, and modulation of cellular signaling pathways. The therapeutic effects often result from synergistic actions of multiple phytochemicals present in the extracts, which can influence various physiological processes.

Pharmacokinetics

The pharmacokinetics of radix extracts are largely dependent on the specific plant source and its constituents. Generally, these compounds are absorbed in the gastrointestinal tract, metabolized primarily by the liver, and excreted via urine or bile. The bioavailability of bioactive compounds can vary, influenced by factors such as the method of preparation, the presence of other food substances, and the individual’s metabolic rate.

Pregnancy

Lack of sufficient data on safety during pregnancy. Caution is advised.

Breast-feeding

Limited data available. Use with caution and consult a healthcare professional.

Storage

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

Indications

• Nutritional supplement
• Support for digestive health
• Enhancement of immune function
• Source of B vitamins

Dosage

Children: Refer to specific product guidelines, as dosage may vary based on formulation and intended use.

Adults: Refer to specific product guidelines, as dosage may vary based on formulation and intended use.

Mechanism of action

Yeast operates through various biochemical pathways, primarily by fermenting sugars to produce alcohol and carbon dioxide. In its role as a dietary supplement, it may enhance gut health by supporting the growth of beneficial gut flora and improving nutrient absorption. Additionally, yeast extract can modulate immune responses and has been studied for its potential antioxidant properties.

Pharmacodynamics

Yeast contains various bioactive compounds, including beta-glucans, which may enhance immune function and exhibit anti-inflammatory properties. The nutrients in yeast, such as B vitamins and amino acids, play crucial roles in metabolic processes, energy production, and overall health maintenance. The fermentation products can also influence gut microbiota composition and enhance digestive health.

Pharmacokinetics

When ingested, yeast components are digested in the gastrointestinal tract where they are broken down into absorbable nutrients. The bioavailability of vitamins and minerals from yeast can vary based on the preparation method. The metabolic byproducts of yeast fermentation are utilized by the body for energy and other metabolic functions. The elimination of yeast components occurs primarily through fecal excretion, as well as through metabolic pathways in the liver.

Adverse effects

• Gastrointestinal discomfort
• Gas and bloating
• Allergic reactions
• Headache

Precautions

• Use with caution in individuals with a compromised immune system
• May cause allergic reactions in sensitive individuals

Pregnancy

Generally considered safe, but consult a healthcare provider before use.

Breast-feeding

Generally considered safe, but consult a healthcare provider before use.

Storage

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

Formulations

• Capsules
• Tablets
• Powder
• Liquid

Mechanism of action

The mechanism of action of acitretin is unknown, however it is believed to work by targeting specific receptors (retinoid receptors such as RXR and RAR) in the skin which help normalize the growth cycle of skin cells.

Pharmacodynamics

Acitretin is a retinoid. Retinoids have a structure similar to vitamin A and are involved in the normal growth of skin cells. Acitretin works by inhibiting the excessive cell growth and keratinisation (process by which skin cells become thickened due to the deposition of a protein within them) seen in psoriasis. It therefore reduces the thickening of the skin, plaque formation and scaling.

Mechanism of action

Beta-carotene is an antioxidant that presents significant efficacy against the reactive oxygen species singlet oxygen. Beta-carotene acts as a scavenger of lipophilic radicals within the membranes of every cell compartments. It also presents an oxidative modification of LDL. The presence of long chains of conjugated double bonds is responsible for its antioxidative properties by allowing beta-carotene to chelate oxygen-free radicals and dissipate their energy. The chelation of free radicals inhibits the peroxidation of lipids. The effect of beta-carotene in the immune response is thought to be related to the direct effect on the thymus which increases the production of immune cells. IN HEMATOPORPHYRIN PHOTOSENSITIZED MICE BETA-CAROTENE SHOWED PHOTOPROTECTION WAS DUE TO FREE RADICAL SCAVENGING OR SINGLET O QUENCHING BUT ALSO A POSSIBLE ROLE OF 400 NM LIGHT ABSORPTION, A PROPERTY OF BETA-CAROTENE. Beta carotene protects patients with erythropoietic protoporphyria against severe photosensitivity reactions (burning sensation, edema, erythema, pruritus, and/or cutaneous lesions). The drug has no effect on the basic biochemical abnormality of erythropoietic protoporphyria (eg, erythrocyte, plasma, and stool concentrations of protoporphyrins are not altered by the drug). The precise mechanism by which the drug exerts photoprotection has not been established. There is some evidence that photosensitizers may act through the formation of singlet excited oxygen and/or free radicals. Since in vitro studies indicate that beta carotene can quench free radicals and singlet excited oxygen, this may be the mechanism by which the drug acts. It is unlikely that beta carotene acts simply as a filter for the wavelengths of light that induce phototoxic effects. beta-Carotene inhibits UV-B carcinogenesis. beta-Carotene is an excellent quencher of singlet oxygen, and can quench free radicals. beta-Carotene has been shown to quench singlet oxygen/free radical reactions in the skin of porphyric mice, and has been found to quench excited species formed on irradiation of mouse skin by UV-B.

Pharmacodynamics

Oral administration of beta-carotene increases the serum concentration of beta-carotene by 60% but it does not change the concentration found in the heart, liver or kidneys. In vitro studies in hepatocytes have shown that beta-carotene ameliorates oxidative stress, enhances antioxidant activity and decreases apoptosis. Other than the antioxidant activities, some other actions have been correlated to beta-carotene. It is thought to have detoxifying properties, as well as to help increase resistance to inflammation and infection and increase immune response and enhance RNA production.

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.

Mechanism of action

Selenium is first metabolized to selenophosphate and selenocysteine. Selenium incorporation is genetically encoded through the RNA sequence UGA. This sequence is recognized by RNA ste loop structures called selenocysteine inserting sequences (SECIS). These structures require the binding of SECIS binding proteins (SBP-2) to recognize selenocystiene. The specialized tRNA is first bound to a serine residue which is then enzymatically processed to a selylcysteyl-tRNA by selenocystiene sythase using selenophosphate as a selenium donor. Other unidentified proteins are required as part of the binding of this tRNA to the ribosome. Selenoproteins appear to be necessary for life as mice with the specialized tRNA gene knocked out exhibited early embryonic lethality. The most important selenoproteins seem to be the glutathione peroxidases and thioredoxin reductases which are part of the body's defenses againts reactive oxygen species (ROS). The importance of selenium in these anti-oxidant proteins has been implicated in the reduction of atherosclerosis by preventing the oxidation of low density lipoprotein. Selenium supplementation is also being investigated in the prevention of cancer and has been suggested to be beneficial to immune function. Converging data from epidemiological, ecological, and clinical studies have shown that selenium (Se) can decrease the risk for some types of human cancers. Induction of apoptosis is considered an important cellular event that can account for the cancer preventive effects of Se. Prior to occurrence of apoptosis, Se compounds alter the expression and/or activities of signaling molecules, mitochondria-associated factors, transcriptional factors, tumor suppressor genes, and cellular reduced glutathione. Mechanistic studies have demonstrated that the methylselenol metabolite pool has many desirable attributes of chemoprevention, whereas the hydrogen selenide pool with excess of selenoprotein synthesis can lead to DNA single-strand breaks. To elucidate the effects of Se on cytotoxic events, it should be remembered that the chemical forms and the dose of Se, and the experimental system used, are determinants of its biological activities. This mini-review focuses on elucidation of the molecular mechanisms of cancer prevention by Se with the apoptotic approach. /Selenium/ Selenium status can also influence thyroid hormone function via the deiodinase enzymes. Selenium is a critical component of the deiodinase enzymes, including iodothyronine 5'-deiodinases, which convert the prohormone thyroxine (T4) to the active circulating form, triiodothyronine (T3). Selenium is also a component of GPX, the main enzyme responsible for protecting thyroid cells against oxidative damage. GPX is involved in the detoxification of hydrogen peroxide, which is produced in the thyroid during the conversion of T4 to T3. /Selenium/ Selenium readily substitutes for sulfur in biomolecules and in many biochemical reactions, especially when the concentration of selenium is high and the concentration of sulfur is low in the organism. Inactivation of the sulfhydryl enzymes necessary for oxidative reactions in cellular respiration, through effects on mitochondrial and microsomal electron transport, might contribute to acute selenium toxicity. Selenium may have a role in hepatic heme metabolism that is related to GPX or lipid peroxidation. Selenocysteine is specifically found in some proteins (e.g., glutathione peroxidase); selenomethionine appears to randomly substitute for methionine in protein synthesis. This appears to be an additional mechanism for intermediate- or chronic-duration toxicity. Skin, hair, and nail damage are significant indicators of chronic selenium overexposure. The mechanism causing these integumentary effects is unclear, but could be related to the high selenium concentrations in these tissues as a consequence of the substitution of selenium for sulfur in certain amino acids, including the disulfide bridges that pr

Pharmacodynamics

Selenium is incorporated into many different selenoproteins which serve various functions throughout the body.

Mechanism of action

Most individuals naturally generate adequate amounts of vitamin D through ordinary dietary intake of vitamin D (in some foods like eggs, fish, and cheese) and natural photochemical conversion of the vitamin D3 precursor 7-dehydrocholesterol in the skin via exposure to sunlight. Conversely, vitamin D deficiency can often occur from a combination of insufficient exposure to sunlight, inadequate dietary intake of vitamin D, genetic defects with endogenous vitamin D receptor, or even severe liver or kidney disease. Such deficiency is known for resulting in conditions like rickets or osteomalacia, all of which reflect inadequate mineralization of bone, enhanced compensatory skeletal demineralization, resultant decreased calcium ion blood concentrations, and increases in the production and secretion of parathyroid hormone. Increases in parathyroid hormone stimulate the mobilization of skeletal calcium and the renal excretion of phosphorus. This enhanced mobilization of skeletal calcium leads towards porotic bone conditions. Ordinarily, while vitamin D3 is made naturally via photochemical processes in the skin, both itself and vitamin D2 can be found in various food and pharmaceutical sources as dietary supplements. The principal biological function of vitamin D is the maintenance of normal levels of serum calcium and phosphorus in the bloodstream by enhancing the efficacy of the small intestine to absorb these minerals from the diet. At the liver, vitamin D3 or D2 is hydroxylated to 25-hydroxyvitamin D and then finally to the primary active metabolite 1,25-dihydroxyvitamin D in the kidney via further hydroxylation. This final metabolite binds to endogenous vitamin d receptors, which results in a variety of regulatory roles - including maintaining calcium balance, the regulation of parathyroid hormone, the promotion of the renal reabsorption of calcium, increased intestinal absorption of calcium and phosphorus, and increased calcium and phosphorus mobilization of calcium and phosphorus from bone to plasma to maintain balanced levels of each in bone and the plasma. In particular, calcitriol interacts with vitamin D receptors in the small intestine to enhance the efficiency of intestinal calcium and phosphorous absorption from about 10-15% to 30-40% and 60% increased to 80%, respectively. Furthermore, calcitriol binds with vitamin D receptors in osteoblasts to stimulate a receptor activator of nuclear factor kB ligand (or RANKL) which subsequently interacts with receptor activator of nuclear factor kB (NFkB) on immature preosteoclasts, causing them to become mature bone-resorbing osteoclasts. Such mature osteoclasts ultimately function in removing calcium and phosphorus from bone to maintain blood calcium and phosphorus levels. Moreover, calcitriol also stimulates calcium reabsorption from the glomerular filtrate in the kidneys. Additionally, it is believed that when calcitriol binds with nuclear vitamin D receptors, that this bound complex itself binds to retinoic acid X receptor (RXR) to generate a heterodimeric complex that consequently binds to specific nucleotide sequences in the DNA called vitamin D response elements. When bound, various transcription factors attach to this complex, resulting in either up or down-regulation of the associated gene's activity. It is thought that there may be as much as 200 to 2000 genes that possess vitamin D response elements or that are influenced indirectly to control a multitude of genes across the genome. It is in this way that cholecalciferol is believed to function in regulating gene transcription associated with cancer risk, autoimmune disorders, and cardiovascular disease linked to vitamin D deficiency. In fact, there has been some research to suggest calcitriol may also be able to prevent malignancies by inducing cellular maturation and inducing apoptosis and inhibiting angiogenesis, exhibit anti-inflammatory effects by inhibiting foam cell formation and promoting angiogenesis in en

Pharmacodynamics

The in vivo synthesis of the predominant two biologically active metabolites of vitamin D occurs in two steps. The first hydroxylation of vitamin D3 cholecalciferol (or D2) occurs in the liver to yield 25-hydroxyvitamin D while the second hydroxylation happens in the kidneys to give 1, 25-dihydroxyvitamin D. These vitamin D metabolites subsequently facilitate the active absorption of calcium and phosphorus in the small intestine, serving to increase serum calcium and phosphate levels sufficiently to allow bone mineralization. Conversely, these vitamin D metabolites also assist in mobilizing calcium and phosphate from bone and likely increase the reabsorption of calcium and perhaps also of phosphate via the renal tubules. There exists a period of 10 to 24 hours between the administration of cholecalciferol and the initiation of its action in the body due to the necessity of synthesis of the active vitamin D metabolites in the liver and kidneys. It is parathyroid hormone that is responsible for the regulation of such metabolism at the level of the kidneys.

Mechanism of action

The mechanism of action of the active metabolite, acitretin, is unknown, however it is believed to work by targeting specific receptors (retinoid receptors) in the skin which help normalize the growth cycle of skin cells.

Pharmacodynamics

The active metabolite responsible for etretinate's effects, acitretin, is a retinoid. Retinoids have a structure similar to vitamin A and are involved in the normal growth of skin cells. Acitretin works by inhibiting the excessive cell growth and keratinisation (process by which skin cells become thickened due to the deposition of a protein within them) seen in psoriasis. It therefore reduces the thickening of the skin, plaque formation and scaling.

Mechanism of action

The biological activity of hydrogen chloride is associated with its high solubility in water i.e., 23 moles/L at 0 °C. ... The hydrogen chloride in water dissociates almost completely, with the hydrogen ion captured by the water molecules to form the hydronium ion. The hydronium ion becomes a donor of a proton that possesses catalytic properties and thus is capable of reacting with organic molecules. This may explain the ability of hydrogen chloride to induce cellular injury and necrosis.