Sequitonic Plus Solution (Each 100ml contains B1 40mg/ liver Extract 1750mg/Saccgharomyces cereuisiae 2.5 *10''cfu/ Alpha amylase 15000mcg/Protein hydrolysate 500mg/Biotin 25mcg/D-panthenol 30mg/Vitamin 12 35mcg/Yeast extreact 600mg/Ascorbic acid 100mg/Dapaine 1500mg/Inositol 300mg/Niacin 300mg/Choline Chloride 30mg)

Indications

• Isolated carboxylase defects
• Defects of biotin metabolism
• Prevention of deficiency in complete biliary obstruction

Dosage

Children: Neonate: Initially 10 mg once daily, adjusted according to response; maintenance 5–20 mg daily. Child: Initially 10 mg once daily, adjusted according to response; maintenance 5–20 mg daily, higher doses may be required.

Adults: For adults, the dosing may vary based on the condition being treated. General guidance is to refer to the BNF for specific dosing recommendations.

Mechanism of action

Biotin acts as a coenzyme for carboxylase enzymes, facilitating critical metabolic processes including gluconeogenesis, fatty acid synthesis, and amino acid catabolism.

Pharmacodynamics

Biotin is essential for the carboxylation of substrates in metabolic pathways, influencing energy metabolism and the synthesis of important biomolecules. It supports normal growth and development.

Pharmacokinetics

Biotin is absorbed in the intestine and is widely distributed in body tissues. It is not stored in large amounts, with excess being excreted in urine. The half-life and specific pharmacokinetic parameters can vary based on individual metabolism and dietary intake.

Adverse effects

• Rough skin
• Dry hair
• Enlarged liver
• Increases in erythrocyte sedimentation rate
• Increased serum calcium
• Increased serum alkaline phosphatase concentration

Precautions

• Excessive doses may be teratogenic
• High levels of vitamin A may cause birth defects

Pregnancy

No information available.

Breast-feeding

No information available.

Formulations

• Tablet
• Oral suspension
• Oral solution
• Solution for injection

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

• Hypertension
• Benign prostatic hyperplasia
• Urinary retention related to prostate enlargement

Dosage

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

Adults: Refer to the BNF for specific dosing recommendations based on individual clinical scenarios.

Mechanism of action

Alpha acts by selectively blocking alpha-1 adrenergic receptors, which are responsible for mediating vasoconstriction in blood vessels. By inhibiting these receptors, alpha promotes vasodilation, leading to a decrease in peripheral vascular resistance and subsequently lowering blood pressure. Additionally, this action can help alleviate urinary symptoms associated with an enlarged prostate.

Pharmacodynamics

The pharmacodynamics of alpha involve its competitive antagonism at alpha-1 adrenergic receptors, resulting in decreased vasoconstriction and increased blood flow. This mechanism is beneficial in conditions characterized by high blood pressure and urinary retention due to prostatic enlargement. The onset of action typically occurs within hours, with peak effects observed within a few days of consistent dosing.

Pharmacokinetics

Alpha is absorbed well from the gastrointestinal tract, with peak plasma concentrations achieved within 1-3 hours post-administration. The drug undergoes hepatic metabolism, primarily via cytochrome P450 enzymes, resulting in active and inactive metabolites. The elimination half-life varies, but it generally is around 6-12 hours, allowing for once-daily dosing in many cases. Renal excretion is a significant route for its metabolites, necessitating caution in patients with renal impairment.

Interactions

• maois, irreversible + alpha blockers: Severe (increases effects)
• ribociclib + alpha blockers: Severe (increases exposure)
• cobicistat + alpha blockers: Moderate (increases exposure)
• idelalisib + alpha blockers: Moderate (increases exposure)
• dronedarone + alpha blockers: Unknown (increases exposure)
• antifungals, azoles + alpha blockers: Unknown (increases exposure)
• crizotinib + alpha blockers: Unknown (increases exposure)
• imatinib + alpha blockers: Unknown (increases exposure)
• letermovir + alpha blockers: Unknown (increases exposure)
• clarithromycin + alpha blockers: Unknown (increases exposure)

Indications

• Pancreatitis
• Salivary gland disorders
• Carbohydrate malabsorption syndromes

Dosage

Children: Refer to the BNF for Children for appropriate dosing information.

Adults: Refer to the specific guidelines and dosing recommendations in the BNF.

Mechanism of action

Amylase facilitates the breakdown of starch and glycogen into maltose and dextrins by cleaving the α-1,4-glycosidic bonds in these polysaccharides. Its action begins in the mouth with salivary amylase and continues in the small intestine with pancreatic amylase, where it further digests carbohydrates.

Pharmacodynamics

Amylase increases the rate of carbohydrate digestion, thereby influencing blood glucose levels. The enzyme's activity can be affected by pH levels, temperature, and the presence of inhibitors or activators. In clinical settings, elevated levels of amylase in the blood can indicate pancreatitis or other pancreatic disorders.

Pharmacokinetics

Amylase is absorbed and metabolized in the gastrointestinal tract. Its activity is measured through serum levels, with normal ranges indicating proper pancreatic function. The half-life of amylase in the bloodstream can vary based on individual metabolic rates and health conditions.

Pregnancy

Amylase is generally considered safe during pregnancy but should be used under medical supervision.

Breast-feeding

Amylase is excreted in breast milk; it is advisable to consult a healthcare provider before use while breastfeeding.

Storage

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

Indications

• Nutritional supplementation
• Support for digestive health
• Enhancement of immune function
• Potential aid in metabolic regulation

Dosage

Children: Refer to clinical guidelines for appropriate dosages in children.

Adults: Refer to clinical guidelines for recommended dosages based on specific formulations and health needs.

Mechanism of action

Cerevisiae functions through various biochemical pathways including the fermentation of sugars to produce ethanol and carbon dioxide. It also contributes to the synthesis of B vitamins and other metabolites that support cellular functions and energy production. Its polysaccharides, notably beta-glucans, can enhance immune responses by activating macrophages and other immune cells.

Pharmacodynamics

The pharmacodynamics of cerevisiae involves its effects on gut health and metabolism. It aids in the fermentation processes that support digestion and can enhance nutrient absorption. The beta-glucans present in the yeast are known to modulate immune system activity and may have antitumor properties, enhancing overall health.

Pharmacokinetics

Cerevisiae is typically consumed orally and is metabolized in the gastrointestinal tract. Its components, such as vitamins and amino acids, are readily absorbed in the intestines. The yeast cells themselves may not be fully digested, but beneficial components are released during the fermentation process. The elimination of metabolites occurs primarily through the urine.

Pregnancy

There is limited information on the use of cerevisiae during pregnancy. Consult a healthcare professional before use.

Breast-feeding

Limited data is available on the excretion of cerevisiae in breast milk. Consult a healthcare professional before use.

Storage

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

Indications

• Choline deficiency
• Support in liver function
• Neurological health, including cognitive function
• Fat metabolism disorders

Dosage

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

Adults: Refer to the BNF for specific dosing guidelines.

Mechanism of action

Choline is a major component of phosphatidylcholine, which is essential for maintaining cell membrane integrity, facilitating information flow, and intracellular communication. It is involved in the synthesis of acetylcholine, a key neurotransmitter in the central nervous system. Choline deficiency can lead to apoptosis by affecting cell membrane composition and increasing ceramide levels, which activates apoptotic pathways. Additionally, choline is a precursor to betaine, which helps regulate homocysteine levels, thus reducing cardiovascular risks.

Pharmacodynamics

Choline is crucial for proper nerve conduction in the central nervous system as it is a precursor for acetylcholine. It supports liver function, gallbladder regulation, and lipid metabolism. Adequate choline levels are associated with the prevention of excessive fat accumulation in the liver and may mitigate conditions such as Parkinsonism and tardive dyskinesia. Deficiencies can lead to serious health problems, including liver dysfunction and stunted growth.

Pharmacokinetics

Choline is absorbed in the intestines and distributed throughout the body, where it is utilized in various metabolic pathways. The liver plays a central role in choline metabolism, converting it into phosphatidylcholine and other metabolites. The half-life and excretion pathways of choline are not well defined but are influenced by dietary intake, physiological state, and individual metabolism.

Interactions

• corticosteroids+cholinesalicylate: Unknown (decreases concentration)

Pregnancy

Choline is generally considered safe during pregnancy, as it is essential for fetal development, particularly for brain development and function. However, it is important to adhere to recommended dietary allowances.

Breast-feeding

Choline is important during breastfeeding as it supports infant brain development. Adequate intake is recommended for nursing mothers.

Storage

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

Indications

• Topical treatment of skin wounds
• Moisturizing dry skin
• Management of minor burns
• Soothing irritations and inflammation of the skin

Dosage

Children: Refer to the BNF for Children for specific dosing

Adults: Apply to the affected area as needed, following the specific product instructions.

Mechanism of action

Dexpanthenol is enzymatically converted to pantothenic acid, which is integral to the formation of coenzyme A. This coenzyme acts as a cofactor in numerous enzymatic reactions, particularly those related to protein metabolism in epithelial tissues. The topical application of dexpanthenol promotes fibroblast proliferation and accelerates wound healing through enhanced re-epithelialization. It also increases the availability of coenzyme A for acetylcholine synthesis, which can enhance intestinal motility by improving peristalsis.

Pharmacodynamics

Dexpanthenol, through its conversion to pantothenic acid, plays a vital role in the synthesis of coenzyme A, which is necessary for various metabolic processes, including the transfer of acetyl groups. It directly influences the production of acetylcholine, the neurotransmitter responsible for parasympathetic nervous system functions, which include maintaining normal intestinal activity. A deficiency in acetylcholine can lead to reduced peristalsis and conditions such as adynamic ileus.

Pharmacokinetics

Dexpanthenol is well absorbed when applied topically. It penetrates the skin effectively, reaching the underlying tissues where it can exert its biological effects. The metabolism of dexpanthenol involves its conversion to pantothenic acid, which further participates in the synthesis of coenzyme A. The elimination half-life and extent of systemic absorption vary based on the formulation and route of administration, but topical use typically results in low systemic exposure.

Adverse effects

• Skin irritation
• Allergic reactions

Precautions

• Use with caution in patients with known allergies to dexpanthenol or related compounds.

Pregnancy

Dexpanthenol is generally considered safe for use during pregnancy, but it is advisable to consult a healthcare provider before use.

Breast-feeding

Dexpanthenol is considered safe during breastfeeding, but consult a healthcare provider for specific recommendations.

Storage

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

Formulations

• Topical cream
• Topical ointment
• Topical solution

Indications

• Type 2 Diabetes Mellitus
• Heart failure (reduced ejection fraction)
• Chronic kidney disease

Dosage

Children: Refer to the BNF for Children for specific pediatric dosing recommendations, as dapagliflozin is not typically indicated for use in

Adults: Refer to relevant clinical guidelines or the BNF for specific dosing recommendations, as dosing may vary based on individual patient factors.

Mechanism of action

Dapagliflozin selectively inhibits the sodium-glucose cotransporter 2 (SGLT2) in the proximal renal tubules. This inhibition reduces glucose reabsorption, leading to increased urinary glucose excretion and decreased blood glucose levels. By decreasing the reabsorption of glucose, dapagliflozin also helps in osmotic diuresis, which may contribute to weight loss and blood pressure reduction.

Pharmacodynamics

The pharmacodynamic effects of dapagliflozin include lowering of blood glucose levels, reduction in body weight, and improvement in glycemic control. It also has favorable effects on blood pressure due to diuresis. Dapagliflozin may provide cardiovascular benefits, as some studies suggest reductions in heart failure hospitalizations, and it may have renal protective effects in patients with chronic kidney disease.

Pharmacokinetics

Dapagliflozin is absorbed rapidly after oral administration, with peak plasma concentrations occurring approximately 1 hour post-dose. It has a bioavailability of about 78%. The drug is primarily metabolized in the liver through UGT2B7 and UGT2B4 glucuronidation pathways, leading to inactive metabolites. The elimination half-life is approximately 12.9 hours, and the drug is primarily excreted through the urine, with about 75% of the dose eliminated as metabolites and about 25% as unchanged drug.

Pregnancy

Dapaine should be used in pregnancy only if the potential benefit justifies the potential risk to the fetus. Consult health care professionals before use.

Breast-feeding

It is not known whether Dapaine is excreted in human milk. Caution should be exercised when administering Dapaine to a nursing woman.

Storage

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

Indications

• General wellness support
• Anti-inflammatory effects
• Antioxidant activity
• Digestive aid
• Support for immune function

Dosage

Children: Paediatric dosing should be determined based on the specific extract and its intended use. Consultation with a healthcare provider is recommended for accurate dosing.

Adults: Dosage varies widely depending on the specific extract and formulation. It is essential to follow the manufacturer's instructions or consult a healthcare professional for appropriate dosing.

Mechanism of action

The mechanism of action of herbal extracts can vary significantly based on their constituents. Commonly, they exert their effects through multiple pathways including modulation of neurotransmitter systems, interference with inflammatory processes, or direct antioxidant activity. Some extracts may activate certain receptors or inhibit enzymes related to disease processes.

Pharmacodynamics

The pharmacodynamics of extracts is complex due to the presence of multiple active compounds which can have synergistic or antagonistic effects. These compounds may influence cellular signaling pathways, alter gene expression, or modulate immune response. The overall pharmacological profile is determined by the specific composition of the extract, its concentration, and the biological target it interacts with.

Pharmacokinetics

The pharmacokinetics of extracts involves absorption, distribution, metabolism, and excretion of the active compounds. Generally, herbal extracts are absorbed in the gastrointestinal tract, with bioavailability influenced by factors such as formulation, the presence of food, and individual metabolic differences. Compounds may undergo hepatic metabolism, and elimination can occur through urine or feces, depending on their chemical nature.

Pregnancy

Consult a healthcare professional before use, as the safety of the extract during pregnancy has not been established.

Breast-feeding

Consult a healthcare professional before use, as the safety of the extract during breastfeeding has not been established.

Storage

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

Dosage

Children: Pediatric dosing for herbal extracts also varies widely and should be approached with caution. Consultation with a healthcare provider is recommended for specific dosing information.

Adults: Dosage for herbal extracts is highly variable and should be determined based on the specific extract and the condition being treated. It is essential to consult specific guidelines or a healthcare professional for appropriate dosing.

Mechanism of action

The mechanism of action for extracts can vary significantly based on the active compounds present in the extract. Generally, many herbal extracts may exert their effects through multiple pathways, including modulation of neurotransmitter systems, anti-inflammatory actions, antioxidant effects, and interactions with various receptors such as GABA, serotonin, and others. Specific mechanisms would depend on the individual extract and its active constituents.

Pharmacodynamics

Pharmacodynamics of herbal extracts often involves the interaction with biological systems at various levels. This can include receptor binding, enzyme modulation, and effects on cellular signaling pathways. The pharmacodynamic profile can be complex, as extracts may contain multiple active compounds that can have synergistic or antagonistic effects on physiological processes.

Pharmacokinetics

Pharmacokinetics of herbal extracts can vary widely based on formulation, route of administration, and the specific active components. Generally, absorption can occur in the gastrointestinal tract, and bioavailability can be influenced by the extract's solubility and stability. Distribution may be affected by protein binding and tissue permeability. Metabolism can occur in the liver, and elimination routes can include renal excretion and fecal elimination, depending on the compounds present.

Pregnancy

The safety of extract during pregnancy has not been established. It is advisable to consult a healthcare professional before use.

Breast-feeding

Caution is advised when using extract while breastfeeding, as it is unknown whether it passes into breast milk. Consultation with a healthcare professional is recommended.

Storage

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

Indications

• Nutritional support in malnourished patients
• Post-operative recovery
• Management of malabsorption syndromes
• Support in conditions requiring enhanced protein intake

Dosage

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

Adults: Refer to specific formulations and BNF guidelines for appropriate dosing.

Mechanism of action

Hydrolysates increase the availability of amino acids and peptides for absorption in the intestines. The smaller size of these molecules compared to whole proteins facilitates their transport across the intestinal wall, allowing for quicker and more effective utilization by the body. This mechanism is particularly beneficial in patients with compromised digestive capabilities.

Pharmacodynamics

The pharmacodynamic effects of hydrolysates involve the supply of essential and non-essential amino acids, which are crucial for various metabolic processes, including protein synthesis, neurotransmitter production, and immune function. The rapid absorption of these peptides can lead to quicker recovery times in malnourished individuals or those undergoing surgical recovery.

Pharmacokinetics

Hydrolysates are rapidly absorbed in the gastrointestinal tract, with peak plasma concentrations occurring shortly after ingestion. The bioavailability of amino acids from hydrolysates is generally higher than that of intact proteins due to their smaller molecular size. The metabolism of amino acids occurs primarily in the liver, where they can be utilized for energy production or incorporated into new proteins. The elimination of amino acids happens through renal pathways, with excess being excreted in urine.

Pregnancy

Safety during pregnancy has not been established. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known if hydrolysate is excreted in human milk. Caution should be exercised when administering to nursing mothers.

Storage

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

Indications

• Polycystic ovary syndrome (PCOS)
• Generalized anxiety disorder
• Depression
• Obsessive-compulsive disorder
• Insulin resistance

Dosage

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

Adults: Refer to the BNF for specific dosing recommendations, as doses may vary based on the condition being treated.

Mechanism of action

Inositol functions primarily as a precursor for the synthesis of phosphoinositides, which are key components of cell membranes. These phosphoinositides are involved in various intracellular signaling pathways, particularly those mediated by G-protein coupled receptors. Inositol also influences the action of neurotransmitters such as serotonin and has been shown to enhance insulin sensitivity and glucose metabolism.

Pharmacodynamics

Inositol has been observed to have mood-stabilizing effects and may improve insulin sensitivity. Its role in cell signaling impacts various physiological processes, including cellular communication and metabolic regulation. The therapeutic effects of inositol in psychiatric conditions may be attributed to its ability to modulate neurotransmitter systems, particularly involving serotonin and dopamine.

Pharmacokinetics

Inositol is well-absorbed from the gastrointestinal tract, with peak plasma levels occurring within 1 to 2 hours after ingestion. It is distributed throughout the body and can cross the blood-brain barrier. Inositol is predominantly excreted in the urine, with a half-life that varies based on dosage and individual metabolism. Metabolism occurs primarily through dephosphorylation to form various inositol phosphates.

Pregnancy

Inositol is generally considered safe during pregnancy but should be used under medical supervision.

Breast-feeding

Inositol is likely safe during breastfeeding, but consult a healthcare provider for specific recommendations.

Storage

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

Formulations

• Powder
• Capsules

Indications

• Liver function tests
• Hepatic encephalopathy
• Liver cirrhosis
• Hepatitis
• Fatty liver disease
• Drug metabolism monitoring

Dosage

Children: Dosing for pediatric patients should always be referenced from established guidelines or the BNF for Children, as it varies significantly based on age, weight, and specific liver-related conditions.

Adults: Dosing for liver-related therapies depends on the specific condition and drug being utilized. Refer to specific drug monographs for detailed dosing information.

Mechanism of action

The liver functions through various pathways, including the hepatic portal system, where nutrients absorbed from the gastrointestinal tract are transported to the liver for processing. Hepatocytes, the functional cells of the liver, engage in metabolic processes such as gluconeogenesis, glycogenolysis, and lipid synthesis. The liver also produces proteins such as albumin and clotting factors, and detoxifies drugs and metabolites through enzymatic reactions involving cytochrome P450 enzymes.

Pharmacodynamics

Pharmacodynamics in relation to liver function often involves the liver's capacity to metabolize drugs and regulate their pharmacological effects. It affects the bioavailability of drugs, their half-life, and overall efficacy. Hepatic dysfunction can lead to altered drug metabolism, resulting in increased drug accumulation and potential toxicity.

Pharmacokinetics

Pharmacokinetics related to liver function involves the absorption, distribution, metabolism, and excretion (ADME) of substances. After oral administration, drugs are absorbed in the gastrointestinal tract and transported via the portal vein to the liver. The liver metabolizes drugs through phase I (oxidation, reduction, hydrolysis) and phase II (conjugation) reactions. Metabolites are then excreted into bile or transported to the kidneys for renal excretion. Factors such as hepatic blood flow, enzyme activity, and liver disease can significantly impact these processes.

Pregnancy

Liver function is crucial during pregnancy, and any liver disease can significantly impact both maternal and fetal health. Careful monitoring and management of liver function are essential.

Breast-feeding

Liver health is important during breastfeeding, as liver function affects the metabolism and clearance of drugs that may be excreted in breast milk.

Storage

Liver tissue should be handled and stored in accordance with laboratory guidelines, ensuring it is preserved properly for analysis or transplantation.

Indications

• Vitamin B3 deficiency
• Hyperlipidemia
• Dyslipidemia

Mechanism of action

Niacin decreases lipids and apolipoprotein B (apo B)-containing lipoproteins by modulating triglyceride synthesis in the liver and inhibiting lipolysis in adipose tissue. It inhibits hepatocyte diacylglycerol acyltransferase-2, preventing the final step of triglyceride synthesis, leading to reduced VLDL production. Additionally, niacin inhibits HDL catabolism receptors, increasing HDL levels and half-life. Acute effects include inhibition of nonesterified fatty acid release from adipocytes and stimulation of prostaglandin release from skin Langerhans cells, although these acute effects diminish over time.

Pharmacodynamics

Niacin is used therapeutically to treat vitamin deficiencies and to manage conditions like hyperlipidemia and dyslipidemia. It effectively reduces levels of VLDL and LDL while increasing HDL levels. Niacin has a wide therapeutic window, with typical oral doses ranging from 500 mg to 2000 mg. Caution is advised in patients with diabetes, renal failure, uncontrolled hypothyroidism, and in elderly patients, particularly when combined with simvastatin or lovastatin, due to an increased risk of myopathy and rhabdomyolysis.

Pharmacokinetics

Niacin is absorbed from the gastrointestinal tract and undergoes hepatic metabolism. It is excreted primarily in the urine. The pharmacokinetics can be affected by factors such as age, renal function, and concomitant medications. Peak plasma concentrations are typically reached within 30 minutes to 2 hours after oral administration, depending on the formulation used.

Contra-indications

• Hypersensitivity to niacin or any of its components
• Active liver disease
• Peptic ulcer disease

Adverse effects

• Flushing
• Itching
• Nausea
• Vomiting
• Diarrhea
• Abdominal pain
• Hepatotoxicity
• Hyperglycemia
• Gout exacerbation

Interactions

• Increased risk of myopathy and rhabdomyolysis with statins such as simvastatin or lovastatin
• May enhance the effects of antihypertensive medications
• Potential interaction with anticoagulants

Precautions

• Caution in patients with diabetes due to potential for hyperglycemia
• Monitor liver function tests periodically during prolonged therapy
• Use with caution in patients with renal impairment
• Elderly patients may be more susceptible to adverse effects

Pregnancy

Niacin should only be used during pregnancy if clearly needed and the benefits outweigh the risks. Consult with a healthcare provider for individual assessment.

Breast-feeding

Niacin is excreted in breast milk. Caution is advised when administering to nursing mothers, and a decision should be made whether to discontinue breastfeeding or the drug.

Storage

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

Formulations

• Immediate-release tablets
• Extended-release tablets
• Sustained-release tablets

Indications

• Nutritional supplementation
• Muscle repair and growth
• Immune support
• Enzyme replacement therapy
• Hormonal regulation

Dosage

Children: Refer to specific product guidelines for dosing information, as protein requirements in children vary based on age, growth stage, and health status.

Adults: Refer to specific product guidelines for dosing information, as protein requirements can vary widely based on individual needs, activity levels, and clinical conditions.

Mechanism of action

Proteins exert their effects primarily through their structure and interactions with other molecules. They can function as enzymes, hormones, and antibodies, and their action is often mediated by binding to specific receptors or substrates, leading to a change in cellular activity or function. For example, enzymes catalyze biochemical reactions, while antibodies bind to antigens to facilitate immune responses.

Pharmacodynamics

The pharmacodynamics of proteins can vary significantly depending on the specific protein being considered. Generally, the effects of proteins are dose-dependent and influenced by their concentration, affinity for targets, and duration of action. Proteins can have a wide range of biological activities, including promoting cellular repair, regulating metabolism, and modulating immune responses.

Pharmacokinetics

The pharmacokinetics of proteins includes their absorption, distribution, metabolism, and excretion (ADME). Proteins are typically digested in the gastrointestinal tract into amino acids before being absorbed into the bloodstream. Once in circulation, proteins can be distributed throughout various tissues. They may have a variable half-life based on their structure and function, and they are primarily metabolized by the liver and excreted via the kidneys. The pharmacokinetic profile can be influenced by factors such as the route of administration and the presence of other substances.

Pregnancy

Generally considered safe, but high protein intake should be monitored to avoid potential risks.

Breast-feeding

Adequate protein intake is critical for lactating women to support milk production and quality.

Storage

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

Indications

• Gastrointestinal disorders
• Diarrhea
• Irritable bowel syndrome (IBS)
• Infection prevention during antibiotic therapy
• Enhancement of immune function

Dosage

Children: Refer to product-specific guidelines, as dosages can vary widely depending on the formulation and intended use.

Adults: Refer to product-specific guidelines, as dosages can vary widely depending on the formulation and intended use.

Mechanism of action

Saccharomyces exerts its effects primarily through the modulation of gut microbiota. It may enhance the intestinal barrier function, produce short-chain fatty acids, and influence immune responses. Its probiotic characteristics help in maintaining a balanced gut flora, which can improve digestion and inhibit the growth of pathogenic bacteria.

Pharmacodynamics

The pharmacodynamics of Saccharomyces involves the fermentation of carbohydrates, leading to the production of ethanol and carbon dioxide, which are beneficial in food production. Additionally, it may have interactions with the gut's immune system, potentially promoting an anti-inflammatory response and enhancing mucosal immunity. The overall effect is a supportive role in gastrointestinal health and nutrient absorption.

Pharmacokinetics

The pharmacokinetics of Saccharomyces are not extensively studied in the same manner as traditional pharmaceuticals. However, it is generally recognized that the yeast cells are not absorbed in the gastrointestinal tract and function locally within the gut. They can survive passage through the digestive system, allowing them to exert their probiotic effects.

Adverse effects

• Bloating
• Gas
• Diarrhea
• Allergic reactions

Precautions

• Use with caution in individuals with a compromised immune system.
• May cause adverse effects in patients with certain allergies.

Pregnancy

There is insufficient reliable information regarding the safety of Saccharomyces during pregnancy. It is advised to consult a healthcare professional before use.

Breast-feeding

Limited data is available on the use of Saccharomyces while breastfeeding. Consult a healthcare professional for guidance.

Storage

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

Formulations

• Capsules
• Powder
• Tablets

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'}

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

Biotin is necessary for the proper functioning of enzymes that transport carboxyl units and fix carbon dioxide, and is required for various metabolic functions, including gluconeogenesis, lipogenesis, fatty acid biosynthesis, propionate metabolism, and catabolism of branched-chain amino acids. In human tissues biotin is a cofactor for the enzymatic carboxylation of four substrates: pyruvate, acetyl coenzyme A (CoA), propionyl CoA, and beta-methylcrotonyl CoA. As such, it plays an important role in both carbohydrate and fat metabolism. Carbon dioxide fixation occurs in a two-step reaction, the first involving binding of carbon dioxide to the biotin moiety of the holoenzyme, and the second involving transfer of the biotin-bound carbon dioxide to an appropriate acceptor. Biotin functions in carbon dioxide fixation reactions in intermediate metabolism, transferring the carboxyl group to acceptor molecules. It acts similarly in decarboxylation reactions. Biotin is essential in human metabolism for its part in the previously described enzymatic steps, in catalyzing deamination of amino acids, and in oleic acid synthesis. Biotin is a cofactor for the enzymatic carboxylation of pyruvate, acetyl coenzyme A (CoA), propionyl CoA, and beta-methylcrotonyl CoA, and, therefore, plays an important role in carbohydrate and fat metabolism. Protein folding in the endoplasmic reticulum (ER) depends on Ca2+; uptake of Ca2+ into the ER is mediated by sarco/endoplasmic reticulum Ca2+-ATPase 3 (SERCA3). The 5'-flanking region of the SERCA3 gene (ATP2A3) contains numerous binding sites for the transcription factors Sp1 and Sp3. Biotin affects the nuclear abundance of Sp1 and Sp3, which may act as transcriptional activators or repressors. Here we determined whether biotin affects the expression of the SERCA3 gene and, thus, protein folding in human lymphoid cells. Jurkat cells were cultured in media containing 0.025 nmol/L biotin (denoted "deficient") or 10 nmol/L biotin ("supplemented"). The transcriptional activity of the full-length human SERCA3 promoter was 50% lower in biotin-supplemented cells compared to biotin-deficient cells. Biotin-dependent repressors bind to elements located 731 to 1312 bp upstream from the transcription start site in the SERCA3 gene. The following suggest that low expression of SERCA3 in biotin-supplemented cells impaired folding of secretory proteins in the ER, triggering unfolded protein response: (i) sequestration of Ca2+ in the ER decreased by 14 to 24% in response to biotin supplementation; (ii) secretion of interleukin-2 into the extracellular space decreased by 75% in response to biotin supplementation; (iii) the nuclear abundance of stress-induced transcription factors increased in response to biotin supplementation; and (iv) the abundance of stress-related proteins such ubiquitin activating enzyme 1, growth arrest and DNA damage 153 gene, X-box binding protein 1 and phosphorylated eukaryotic translation initiation factor 2alpha increased in response to biotin supplementation. Collectively, this study suggests that supplements containing pharmacological doses of biotin may cause cell stress by impairing protein folding in the ER. Evidence is emerging that biotin participates in processes other than classical carboxylation reactions. Specifically, novel roles for biotin in cell signaling, gene expression, and chromatin structure have been identified in recent years. Human cells accumulate biotin by using both the sodium-dependent multivitamin transporter and monocarboxylate transporter 1. These transporters and other biotin-binding proteins partition biotin to compartments involved in biotin signaling: cytoplasm, mitochondria, and nuclei. The activity of cell signals such as biotinyl-AMP, Sp1 and Sp3, nuclear factor (NF)-kappaB, and receptor tyrosine kinases depends on biotin supply. Consistent with a role for biotin and its catabolites in modulating these cell signals, greater than 2000 biotin-dependent genes have

Pharmacodynamics

Biotin is a water-soluble B-complex vitamin which is composed of an ureido ring fused with a tetrahydrothiophene ring, which attaches a valeric acid substituent at one of its carbon atoms. Biotin is used in cell growth, the production of fatty acids, metabolism of fats, and amino acids. It plays a role in the Kreb cycle, which is the process in which energy is released from food. Biotin not only assists in various metabolic chemical conversions, but also helps with the transfer of carbon dioxide. Biotin is also helpful in maintaining a steady blood sugar level. Biotin is often recommended for strengthening hair and nails. Consequenty, it is found in many cosmetic and health products for the hair and skin. Biotin deficiency is a rare nutritional disorder caused by a deficiency of biotin. Initial symptoms of biotin deficiency include: Dry skin, Seborrheic dermatitis, Fungal infections, rashes including erythematous periorofacial macular rash, fine and brittle hair, and hair loss or total alopecia. If left untreated, neurological symptoms can develop, including mild depression, which may progress to profound lassitude and, eventually, to somnolence; changes in mental status, generalized muscular pains (myalgias), hyperesthesias and paresthesias. The treatment for biotin deficiency is to simply start taking some biotin supplements. A lack of biotin in infants will lead to a condition called seborrheic dermatitis or "cradle cap". Biotin deficiencies are extremely rare in adults but if it does occur, it will lead to anemia, depression, hair loss, high blood sugar levels, muscle pain, nausea, loss of appetite and inflamed mucous membranes.

Mechanism of action

Choline is a major part of the polar head group of phosphatidylcholine. Phosphatidylcholine's role in the maintenance of cell membrane integrity is vital to all of the basic biological processes: information flow, intracellular communication and bioenergetics. Inadequate choline intake would negatively affect all these processes. Choline is also a major part of another membrane phospholipid, sphingomyelin, also important for the maintenance of cell structure and function. It is noteworthy and not surprising that choline deficiency in cell culture causes apoptosis or programmed cell death. This appears to be due to abnormalities in cell membrane phosphatidylcholine content and an increase in ceramide, a precursor, as well as a metabolite, of sphingomyelin. Ceramide accumulation, which is caused by choline deficiency, appears to activate Caspase, a type of enzyme that mediates apoptosis. Betaine or trimethylglycine is derived from choline via an oxidation reaction. Betaine is one of the factors that maintains low levels of homocysteine by resynthesizing L-methionine from homocysteine. Elevated homocysteine levels are a significant risk factor for atherosclerosis, as well as other cardiovascular and neurological disorders. Acetylcholine is one of the major neurotransmitters and requires choline for its synthesis. Adequate acetylcholine levels in the brain are believed to be protective against certain types of dementia, including Alzheimer's disease.

Pharmacodynamics

This compound is needed for good nerve conduction throughout the CNS (central nervous system) as it is a precursor to acetylcholine (ACh). Choline is also needed for gallbladder regulation, liver function and lecithin (a key lipid) formation. Choline also aids in fat and cholesterol metabolism and prevents excessive fat build up in the liver. Choline has been used to mitigate the effects of Parkinsonism and tardive dyskinesia. Choline deficiencies may result in excessive build-up of fat in the liver, high blood pressure, gastric ulcers, kidney and liver dysfunction and stunted growth.

Mechanism of action

Dexpanthenol is an alcohol derivative of pantothenic acid, a component of the B complex vitamins and an essential component of a normally functioning epithelium. Dexpanthenol is enzymatically cleaved to form pantothenic acid, which is an essential component of Coenzyme A, which acts as a cofactor in many enzymatic reactions that are important for protein metabolism in the epithelium. Dermatological effects of the topical use of dexpanthenol include increased fibroblast proliferation and accelerated re-epithelialization in wound healing. Furthermore, it acts as a topical protectant, moisturizer, and has demonstrated anti-inflammatory properties. This alcohol ... is said to increase the amount of coenzyme A available for the synthesis of acetylcholine. Increased formation of acetylcholine is thought to increase peristalsis and intestinal tone. ... To test the functional effect of pantothenate on dermal fibroblasts, cells were cultured and in vitro proliferation tests were performed using a standardized scratch test procedure. For all three donors analyzed, a strong stimulatory effect of pantothenate at a concentration of 20 ug/mL on the proliferation of cultivated dermal fibroblasts was observed. To study the molecular mechanisms resulting in the proliferative effect of pantothenate, gene expression was analyzed in dermal fibroblasts cultivated with 20 ug/mL of pantothenate compared with untreated cells using the GeneChip Human Exon 1.0 ST Array. A number of significantly regulated genes were identified including genes coding for interleukin (IL)-6, IL-8, Id1, HMOX-1, HspB7, CYP1B1 and MARCH-II. Regulation of these genes was subsequently verified by quantitative real-time polymerase chain reaction analysis. Induction of HMOX-1 expression by pantothenol and pantothenic acid in dermal cells was confirmed on the protein level using immunoblots. Functional studies revealed the enhanced suppression of free radical formation in skin fibroblasts cultured with panthenol. In conclusion, these studies provided new insight in the molecular mechanisms linked to the stimulatory effect of pantothenate and panthenol on the proliferation of dermal fibroblasts. /Calcium pantotenate/ ... Pantothenic acid, pantothenol and other derivatives ... are precursors of CoA /that/ protect cells and whole organs against peroxidative damage by increasing the content of cell glutathione...

Pharmacodynamics

Pantothenic acid is a precursor of coenzyme A, which serves as a cofactor for a variety of enzyme-catalyzed reactions involving transfer of acetyl groups. The final step in the synthesis of acetylcholine consists of the choline acetylase transfer of acetyl group from acetylcoenzyme A to choline. Acetylcholine is the neurohumoral transmitter in the parasympathetic system and as such maintains the normal functions of the intestine. Decrease in acetylcholine content would result in decreased peristalsis and in extreme cases adynamic ileus.

Mechanism of action

Niacin performs a number of functions in the body and so has many mechanisms, not all of which have been fully described. Niacin can decrease lipids and apolipoprotein B (apo B)-containing lipoproteins by modulating triglyceride synthesis in the liver, which degrades apo B, or by modulating lipolysis in adipose tissue. Niacin inhibits hepatocyte diacylglycerol acyltransferase-2. This action prevents the final step of triglyceride synthesis in hepatocytes, limiting available triglycerides for very low density lipoproteins (VLDL). This activity also leads to intracellular degradation of apo B and decreased production of low density lipoproteins, the catabolic product of VLDL. Niacin also inhibits a high density lipoprotein (HDL) catabolism receptor, which increases the levels and half life of HDL. Prolonged niacin treatment elicits beneficial effects on the plasma lipid and lipoprotein profile that is associated with a protective CVD risk profile. Acute niacin treatment inhibits nonesterified fatty acid release from adipocytes and stimulates prostaglandin release from skin Langerhans cells, but the acute effects diminish upon prolonged treatment, while the beneficial effects remain. To gain insight in the prolonged effects of niacin on lipid metabolism in adipocytes, we used a mouse model with a human-like lipoprotein metabolism and drug response [female APOE*3-Leiden.CETP (apoE3 Leiden cholesteryl ester transfer protein) mice] treated with and without niacin for 15 weeks. The gene expression profile of gonadal white adipose tissue (gWAT) from niacin-treated mice showed an upregulation of the "biosynthesis of unsaturated fatty acids" pathway, which was corroborated by quantitative PCR and analysis of the FA ratios in gWAT. Also, adipocytes from niacin-treated mice secreted more of the PUFA DHA ex vivo. This resulted in an increased DHA/arachidonic acid (AA) ratio in the adipocyte FA secretion profile and in plasma of niacin-treated mice. Interestingly, the DHA metabolite 19,20-dihydroxy docosapentaenoic acid (19,20-diHDPA) was increased in plasma of niacin-treated mice. Both an increased DHA/AA ratio and increased 19,20-diHDPA are indicative for an anti-inflammatory profile and may indirectly contribute to the atheroprotective lipid and lipoprotein profile associated with prolonged niacin treatment. /The study objective was/ to determine the effects of niacin on adiponectin and markers of adipose tissue inflammation in a mouse model of obesity. Male C57BL/6 mice were placed on a control or high-fat diet (HFD) and were maintained on such diets for the duration of the study. After 6 weeks on the control or high fat diets, vehicle or niacin treatments were initiated and maintained for 5 weeks. Identical studies were conducted concurrently in HCA2 (-/-) (niacin receptor(-/-)) mice. Niacin increased serum concentrations of the anti-inflammatory adipokine, adiponectin by 21% in HFD-fed wild-type mice, but had no effect on lean wild-type or lean or HFD-fed HCA2 (-/-) mice. Niacin increased adiponectin gene and protein expression in the HFD-fed wild-type mice only. The increases in adiponectin serum concentrations, gene and protein expression occurred independently of changes in expression of PPARgamma C/EBPalpha or SREBP-1c (key transcription factors known to positively regulate adiponectin gene transcription) in the adipose tissue. Further, niacin had no effect on adipose tissue expression of ERp44, Ero1-Lalpha, or DsbA-L (key ER chaperones involved in adiponectin production and secretion). However, niacin treatment attenuated HFD-induced increases in adipose tissue gene expression of MCP-1 and IL-1beta in the wild-type HFD-fed mice. Niacin also reduced the expression of the pro-inflammatory M1 macrophage marker CD11c in HFD-fed wild-type mice. Niacin treatment attenuates obesity-induced adipose tissue inflammation through increased adiponectin and anti-inflammatory cytokine expression and reduced pro-inflammatory cytokine expressio

Pharmacodynamics

Niacin is a B vitamin used to treat vitamin deficiencies as well as hyperlipidemia, dyslipidemia, hypertriglyceridemia, and to reduce the risk of myocardial infarctions. Niacin acts to decrease levels of very low density lipoproteins and low density lipoproteins, while increasing levels of high density lipoproteins. Niacin has a wide therapeutic window with usual oral doses between 500mg and 2000mg. Patients with diabetes, renal failure, uncontrolled hypothyroidism, and elderly patients taking niacin with simvastatin or lovastatin are at increased risk of myopathy and rhabdomyolysis.