BORONOX TABLETS

Indications

• Cognitive impairment
• Dementia
• Memory enhancement
• Anxiety
• Peripheral vascular disease

Dosage

Children: Safety and efficacy in children have not been established. Use is not generally recommended without professional guidance.

Adults: Refer to specific product guidelines, as Ginkgo biloba is available in various forms including tablets, extracts, and teas. Typical doses range from 120 to 240 mg per day, divided into two or three doses.

Mechanism of action

The exact mechanism of action of Ginkgo biloba is not fully understood, but it is believed to enhance cerebral blood flow and improve circulation by inhibiting platelet-activating factor (PAF) and promoting vasodilation through nitric oxide release. Additionally, the antioxidant properties of flavonoids and terpenoids may protect neurons from oxidative stress and free radical damage.

Pharmacodynamics

Ginkgo biloba exhibits several pharmacodynamic effects, including increased blood flow to the brain, improved oxygen utilization, and enhanced glucose metabolism. It may also modulate neurotransmitter systems, including serotonin and dopamine, which could contribute to its effects on mood and cognitive function. The anti-inflammatory properties may further aid in neuroprotection.

Pharmacokinetics

Ginkgo biloba extracts are well-absorbed after oral administration. The bioavailability of its active constituents varies, and peak plasma concentrations occur within 1 to 4 hours post-ingestion. The elimination half-life of ginkgo flavonoids is approximately 4 to 5 hours, and metabolites are primarily excreted in urine. Factors such as age, health status, and concurrent medications can affect its pharmacokinetics.

Adverse effects

• Headache
• Dizziness
• Gastrointestinal upset
• Allergic skin reactions
• Palpitations

Interactions

• Anticoagulants (e.g., warfarin)
• Antiplatelet agents (e.g., aspirin)
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Certain antidepressants (e.g., selective serotonin reuptake inhibitors)

Precautions

• Use with caution in patients with bleeding disorders
• Monitor for potential interactions with other medications
• Discontinue use prior to surgery to reduce bleeding risk

Pregnancy

Not recommended due to insufficient safety data.

Breast-feeding

Lack of sufficient data, caution is advised.

Storage

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

Formulations

• Tablets
• Capsules
• Liquid extracts

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

• Menopausal symptoms
• Osteoporosis prevention
• Cardiovascular health
• Hormonal balance

Dosage

Children: Refer to established guidelines or consult a healthcare provider for specific dosing recommendations.

Adults: Refer to established guidelines or consult a healthcare provider for specific dosing recommendations.

Mechanism of action

The active compounds in clover, particularly in red clover, include isoflavones such as genistein and daidzein. These phytoestrogens can bind to estrogen receptors in the body, exerting estrogen-like effects. This mechanism may help alleviate menopausal symptoms by mimicking the effects of estrogen, thus potentially reducing hot flashes and improving bone health.

Pharmacodynamics

Clover's isoflavones have antioxidant properties and may influence various biological pathways, including modulation of lipid metabolism and inhibition of certain inflammatory processes. The estrogenic activity of these compounds can lead to alterations in hormone levels, which may contribute to its therapeutic effects in postmenopausal women.

Pharmacokinetics

The bioavailability of isoflavones from clover can vary based on the formulation and individual metabolism. After ingestion, isoflavones are metabolized in the liver and can be excreted in urine as conjugated metabolites. Peak plasma concentrations typically occur within a few hours of consumption, and the half-life can vary depending on the specific isoflavone and individual factors.

Adverse effects

• Allergic reactions
• Gastrointestinal upset
• Headaches
• Fatigue

Interactions

• May interact with anticoagulants such as warfarin, increasing the risk of bleeding
• Can affect the efficacy of oral contraceptives
• May interact with other medications metabolized by the liver

Precautions

• Use with caution in individuals with clotting disorders
• Monitor for potential allergic reactions
• Consult healthcare professionals before use in conjunction with other medications

Pregnancy

There is insufficient reliable information regarding the safety of clover during pregnancy; consult a healthcare professional before use.

Breast-feeding

Consult a healthcare professional before using clover while breastfeeding, as safety has not been established.

Storage

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

Formulations

• Dried leaves
• Extracts
• Capsules
• Teas

Indications

• Skin aging and wrinkle reduction
• Joint pain and osteoarthritis
• Tendon and ligament injuries
• Bone health
• Wound healing

Dosage

Children: Refer to specific product guidelines or consult a healthcare professional for appropriate dosing based on the indication and formulation used.

Adults: Refer to specific product guidelines or consult a healthcare professional for appropriate dosing based on the indication and formulation used.

Mechanism of action

Collagen exerts its effects primarily by providing the necessary amino acids, such as glycine, proline, and hydroxyproline, that are crucial for the synthesis of new collagen in the body. It is thought to stimulate fibroblast proliferation, which leads to increased collagen production and improved tissue repair. Additionally, collagen may enhance the hydration of the skin and improve its elasticity.

Pharmacodynamics

Collagen supplementation may promote the synthesis of new collagen and improve the integrity of the extracellular matrix. This can lead to improved skin hydration, elasticity, and the reduction of wrinkles. In joint health, collagen may help reduce inflammation and pain, contributing to improved mobility and function. The effects can vary based on the source of collagen (bovine, porcine, marine) and the form of administration (powder, liquid, capsules).

Pharmacokinetics

After oral administration, collagen peptides are absorbed in the gastrointestinal tract and enter the bloodstream. They can be transported to various tissues where they may be incorporated into the extracellular matrix. The half-life of collagen peptides is relatively short, and they are metabolized in the liver and other tissues. The bioavailability of collagen can vary based on the formulation and the presence of other dietary components.

Adverse effects

• Allergic reactions
• Skin rash
• Itching
• Gastrointestinal disturbances
• Nausea

Precautions

• Use with caution in individuals with fish allergies if derived from fish sources
• Monitor for allergic reactions

Pregnancy

Collagen is generally considered safe during pregnancy, but consult a healthcare professional before use.

Breast-feeding

Collagen is likely safe during breastfeeding, but consult a healthcare professional before use.

Storage

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

Formulations

• Powder
• Capsules
• Liquid

Indications

• Prevention of urinary tract infections
• Supportive treatment for urinary tract health

Dosage

Children: Refer to product guidelines and consult healthcare professionals for appropriate dosing in children.

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

Mechanism of action

Cranberry's primary mechanism of action involves the presence of proanthocyanidins, which prevent the adherence of uropathogenic E. coli to the uroepithelial cells. This reduces the ability of the bacteria to colonize and cause infection. Additionally, cranberry may have antioxidant properties, contributing to its overall health benefits.

Pharmacodynamics

Cranberry demonstrates antibacterial activity specifically against uropathogenic strains of bacteria. The proanthocyanidins in cranberry have been shown to alter the properties of bacterial fimbriae, thereby interfering with their ability to adhere to the bladder wall. This action helps reduce the incidence of urinary tract infections. Furthermore, cranberry may exert a mild diuretic effect, promoting increased urine flow.

Pharmacokinetics

Cranberry components, particularly its polyphenols, undergo extensive metabolism in the gastrointestinal tract. After ingestion, they are absorbed and metabolized in the liver, where they can be excreted in the urine. Peak plasma concentrations of cranberry constituents occur within 1 to 2 hours post-ingestion. Elimination half-lives vary depending on the specific compound and individual metabolism.

Adverse effects

• Gastrointestinal upset
• Diarrhea
• Nausea
• Allergic reactions

Interactions

• May interact with warfarin, potentially increasing bleeding risk
• May alter the effectiveness of certain medications metabolized by the liver

Precautions

• Use with caution in patients with a history of kidney stones
• Monitor for potential interactions with anticoagulants

Pregnancy

Cranberry is generally regarded as safe during pregnancy when consumed in food amounts. However, consult a healthcare provider for supplementation.

Breast-feeding

Cranberry is likely safe during breastfeeding when consumed as food. Consult a healthcare provider for higher doses.

Storage

Store in a cool, dry place away from direct sunlight. Refrigerate after opening if in juice form.

Formulations

• Dried cranberries
• Cranberry juice
• Cranberry extract capsules
• Cranberry tablets

Indications

• Premenstrual syndrome (PMS)
• Eczema (atopic dermatitis)
• Rheumatoid arthritis
• Breast pain (mastalgia)
• Menopausal symptoms

Dosage

Children: Refer to established guidelines or consult a healthcare professional for appropriate dosing in children. Specific dosing recommendations are not well established.

Adults: Refer to established guidelines or consult a healthcare professional for appropriate dosing. Typical doses range from 500 mg to 3000 mg of evening primrose oil per day, depending on the condition being treated.

Mechanism of action

Evening primrose oil exerts its effects primarily through the presence of gamma-linolenic acid (GLA). GLA is converted in the body into prostaglandins, which are compounds that help regulate inflammation and other physiological processes. By increasing the levels of prostaglandins, GLA may help to alleviate symptoms associated with inflammation and hormonal imbalances.

Pharmacodynamics

The pharmacodynamic effects of evening primrose oil are attributed to its fatty acid composition, particularly GLA. It has been shown to modulate inflammatory responses, enhance skin barrier function, and may influence hormonal regulation, providing symptomatic relief in conditions like PMS and eczema. The anti-inflammatory effect may also contribute to its use in managing conditions like rheumatoid arthritis.

Pharmacokinetics

Evening primrose oil is absorbed in the gastrointestinal tract and metabolized by the liver. The bioavailability of GLA may vary among individuals and can be influenced by dietary factors. The half-life of GLA is not well-defined in the literature. The oil is generally well-tolerated, but gastrointestinal side effects may occur in some users.

Pregnancy

Limited data is available on the use of evening primrose oil during pregnancy. Caution is advised.

Breast-feeding

Evening primrose oil is generally considered safe during breastfeeding, but consult a healthcare provider for personalized advice.

Storage

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

Indications

• Cognitive enhancement
• Memory disorders
• Tinnitus
• Peripheral vascular disease
• Anxiety
• Age-related macular degeneration

Dosage

Children: Safety and efficacy have not been established in children, so refer to specific guidelines if considering use in paediatric populations.

Adults: Refer to specific product guidelines, typically ranging from 120 to 240 mg of standardized ginkgo extract per day, divided into two or three doses.

Mechanism of action

The exact mechanism of action of ginkgo is not fully understood, but it is thought to involve several pathways. Ginkgo extracts contain flavonoids and terpenoids, which are believed to contribute to its pharmacological effects. These compounds may enhance cerebral blood flow by dilating blood vessels and reducing blood viscosity. Ginkgo also has antioxidant properties that help protect against oxidative stress, and it may modulate neurotransmitter systems, particularly those involving serotonin and dopamine.

Pharmacodynamics

Ginkgo exhibits various pharmacodynamic effects, including vasodilation, increased blood flow, and improved neurotransmission. It is noted for its ability to enhance cognitive function, particularly in older adults with mild cognitive impairment. The antioxidant properties of ginkgo help mitigate damage caused by free radicals, potentially reducing the risk of neurodegenerative diseases. Its effects on blood circulation can also alleviate symptoms associated with peripheral vascular disease.

Pharmacokinetics

Ginkgo is rapidly absorbed after oral administration, with peak plasma concentrations typically occurring within 1-3 hours. It undergoes extensive metabolism in the liver, primarily via cytochrome P450 enzymes. The elimination half-life of ginkgo components can vary, generally ranging from 4 to 12 hours. The bioavailability of ginkgo extracts can be influenced by formulation and individual patient factors, including age and health status.

Contra-indications

• Hypersensitivity to ginkgo or any of its components
• Active bleeding disorders
• Concurrent use with anticoagulants or antiplatelet agents

Adverse effects

• Gastrointestinal upset
• Headache
• Dizziness
• Allergic skin reactions
• Palpitations

Interactions

• Increased risk of bleeding when used with warfarin, aspirin, or other anticoagulants
• Potential interaction with selective serotonin reuptake inhibitors (SSRIs) and other antidepressants
• May affect the metabolism of certain drugs metabolized by cytochrome P450 enzymes

Precautions

• Use with caution in patients with a history of seizures
• Monitor for bleeding complications in patients with bleeding disorders
• Discontinue use prior to surgical procedures to reduce bleeding risk

Pregnancy

Limited data available, caution advised; consult healthcare provider.

Breast-feeding

Insufficient reliable information available regarding safety; consult healthcare provider.

Storage

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

Formulations

• Ginkgo biloba extract (standardized)
• Ginkgo leaf tablets
• Ginkgo capsules
• Ginkgo tinctures

Indications

• Wound healing
• Skin ulceration
• Burns
• Psoriasis
• Dermatitis

Dosage

Children: Refer to the BNF for Children for appropriate dosing information based on the child's age and condition.

Adults: Refer to the BNF for specific formulations and dosing guidelines, as dosages may vary based on the condition being treated and the formulation used.

Mechanism of action

While there is no well-controlled data to formally substantiate the method of action, ongoing studies suggest that allantoin may induce a histological wound healing profile in animal models, leading to improved reestablishment of normal skin. This includes increased vasodilation, inflammatory cell presence, angiogenesis, fibroblast proliferation, and collagen deposition in treated wounds compared to untreated ones.

Pharmacodynamics

There is limited controlled data regarding the pharmacodynamic properties of allantoin. However, studies indicate that allantoin may possess moisturizing and keratolytic effects, increasing the extracellular matrix's water content and enhancing the desquamation of dead skin cells. These activities can promote cell proliferation and facilitate wound healing.

Pharmacokinetics

Specific pharmacokinetic data for allantoin in humans is limited. However, it is known to be applied topically, which suggests local absorption at the site of application. Systemic absorption is considered minimal due to its low molecular weight and hydrophilicity.

Pregnancy

There is limited data on the safety of allantoin in pregnancy. It is advisable to consult a healthcare professional before use.

Breast-feeding

Allantoin is generally considered safe during breastfeeding, but caution is recommended. Consult a healthcare professional before use.

Storage

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

Formulations

• Topical cream
• Gel
• Ointment

Indications

• Menopausal symptoms
• Cardiovascular health
• Bone health
• Estrogen-dependent cancers

Dosage

Children: Use in children is not

Adults: Dosage varies based on the specific formulation and indication. Refer to the specific product guidelines or the BNF for detailed dosing recommendations.

Mechanism of action

Isoflavones are selective estrogen receptor modulators that exert estrogenic-like effects under certain conditions. They bind preferentially to estrogen receptor beta (ERβ) with a binding affinity approximately 20 times higher than that to estrogen receptor alpha (ERα). Isoflavones can exhibit antiestrogenic actions by blocking the binding of endogenous estrogens and their receptor signaling. They may inhibit the proliferation of breast cancer cells by arresting cell cycle progression and inducing apoptosis. Additionally, isoflavones may act on androgen receptors to inhibit tyrosine kinase activity, blocking cancer cell growth.

Pharmacodynamics

Isoflavones, particularly from soy, have been shown to lower LDL cholesterol levels and improve blood pressure in women with hypertension. In postmenopausal women, dietary intake of isoflavones has been associated with reduced bone resorption and increased bone formation markers. Their effects on menopausal symptoms, breast cancer, and prostate cancer remain controversial, though some studies suggest they may decrease cancer development markers in prostate cells.

Pharmacokinetics

Isoflavones are metabolized in the gut and liver, leading to various bioactive metabolites. Their bioavailability can be affected by dietary factors and individual metabolism. Peak plasma concentrations occur about 2 to 4 hours after ingestion, with a half-life that varies depending on the specific isoflavone and individual factors. Isoflavones are primarily excreted via urine.

Adverse effects

• gastrointestinal disturbances
• allergic reactions
• headaches
• fatigue
• dizziness

Interactions

• may interact with anticoagulants, potentially increasing bleeding risk
• may affect the metabolism of certain medications via CYP450 enzymes
• estrogenic drugs may exhibit compounded effects when used with isoflavones

Precautions

• use cautiously in individuals with hormone-sensitive conditions
• monitor patients with a history of breast or prostate cancer
• consider potential interactions with other medications

Pregnancy

Isoflavones should be used with caution during pregnancy due to their estrogen-like effects; consult healthcare professionals for guidance.

Breast-feeding

Limited data is available; consult healthcare professionals before use during breastfeeding.

Storage

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

Formulations

• capsules
• tablets
• powdered supplements
• soy-based food products

Indications

• Pain relief
• Inflammatory conditions
• Dental applications
• Antifungal treatments
• Antioxidant support

Dosage

Children: Refer to specific product guidelines for pediatric dosing as it may vary based on formulation and intended use.

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

Mechanism of action

The exact mechanism of action of eugenol is not fully understood. However, it has been shown to interrupt action potentials, contributing to its analgesic properties. Eugenol exhibits anti-inflammatory effects by modulating the activity of polymorphonuclear leukocytes, which release inflammatory mediators. Additionally, eugenol has demonstrated antioxidant activity, protecting cells from oxidative stress. It has been observed to inhibit the formation of malondialdehyde in irradiated thymocytes, suggesting a protective role against oxidative damage.

Pharmacodynamics

Eugenol exhibits several pharmacological properties, including analgesic, anti-inflammatory, antipyretic, neuroprotective, antifungal, and antioxidant effects. Its ability to inhibit reactive oxygen species generation and modulate inflammatory mediators contributes to its therapeutic potential in managing pain and inflammation. The dose-dependent effects of eugenol on respiratory inhibition of mitochondria highlight its impact on cellular energy metabolism, further extending its pharmacodynamic profile.

Pharmacokinetics

Eugenol is rapidly absorbed and distributed throughout the body following administration. It undergoes extensive metabolism in the liver, with various metabolic pathways including conjugation and oxidation. The elimination half-life and specific pharmacokinetic parameters can be influenced by the route of administration and individual patient factors. The exact pharmacokinetics of eugenol in humans require further elucidation through clinical studies.

Adverse effects

• Nausea
• Vomiting
• Diarrhea
• Skin irritation
• Allergic reactions

Precautions

• Use with caution in individuals with liver disease or gastrointestinal disorders.
• Caution is advised in patients who are pregnant or breastfeeding.

Pregnancy

Eugenol should be used with caution during pregnancy due to insufficient data on safety.

Breast-feeding

Eugenol is excreted in breast milk; caution is advised when administering to breastfeeding mothers.

Storage

Store in a tightly closed container, in a cool, dry place away from light.

Formulations

• Essential oil
• Topical preparations

Indications

• Eczema
• Premenstrual syndrome (PMS)
• Rheumatoid arthritis
• Menopausal symptoms
• Skin disorders

Dosage

Children: Refer to specific product guidelines, as dosages can vary based on formulation and indication.

Adults: Refer to specific product guidelines, as dosages can vary based on formulation and indication.

Mechanism of action

Gamma-linolenic acid (GLA) is metabolized to prostaglandin E1, which exerts anti-inflammatory effects. This pathway involves the conversion of GLA to dihomo-gamma-linolenic acid (DGLA), which is a precursor for the synthesis of anti-inflammatory prostaglandins, helping to modulate inflammatory responses in the body.

Pharmacodynamics

GLA is thought to alter the metabolism of arachidonic acid, leading to decreased production of pro-inflammatory eicosanoids. This can help alleviate symptoms associated with inflammatory conditions, and the fatty acids present in primrose may also contribute to skin barrier function and hydration, making it beneficial for skin-related disorders.

Pharmacokinetics

After oral administration, GLA is absorbed in the gastrointestinal tract, with peak plasma concentrations typically occurring within a few hours. It is then distributed throughout the body, where it can be incorporated into cell membranes. The metabolism of GLA involves conversion into various metabolites, including DGLA, and it is excreted mainly through urine and feces. The half-life of GLA can vary based on individual metabolism and dietary factors.

Adverse effects

• Gastrointestinal upset
• Nausea
• Diarrhea
• Headache
• Allergic skin reactions

Interactions

• May enhance the effects of anticoagulants
• May interact with antipsychotic medications

Precautions

• Use with caution in individuals with bleeding disorders
• Monitor for potential allergic reactions

Pregnancy

Safety during pregnancy has not been established. Consult a healthcare provider before use.

Breast-feeding

Safety during breastfeeding has not been established. Consult a healthcare provider before use.

Storage

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

Formulations

• Oil
• Capsules
• Tablets

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

There is no well controlled data that can formally substantiate the method of action. However, ongoing studies suggest that there may exist a histological wound healing profile induced by allantoin in rats that leads to the amelioration and fastening of the reestablishment of normal skin. This facilitation of wound healing is supported by observations that wounds inflicted to rat subjects to which topical allantoin preparations were applied histologically demonstrated increased vasodilation, presence of inflammatory exudates, number of inflammatory cells, angiogenesis, fibroblast proliferation, and increased collagen deposition when compared to rat subjects with wounds that did not receive any allantoin administration.

Pharmacodynamics

There is no well controlled and appropriate data that can formally substantiate the pharmacodynamic properties of allantoin. Nevertheless, ongoing studies suggest that allantoin possesses moisturizing and keratolytic effects, as well as abilities to increase the water content of the extracellular matrix and enhance the desquamation of upper layers of dead skin cells, all of which are activities that can promote cell proliferation and facilitate wound healing.

Mechanism of action

Isoflavones are selective estrogen receptor modulators that exert estrogenic-like effects under certain experimental conditions, as they are structurally similar to mammalian 17β-estradiol. They may bind to both α and β isoforms of estrogen receptor (ER), but with binding affinities to ERβ approximately 20 times higher than that to ERα. The role of isoflavones on estrogen-dependent cancer has been studied, since they may mediate antiestrogenic actions by blocking the binding of endogenous estrogens and their receptor signalling. In cell culture, [DB01645] inhibited the proliferation of MDA-MB-231 human breast cancer cells, probably by arresting the cell cycle progression at the G2–M transition. In addition, genistein was shown to induce apoptosis, modify eicosanoid metabolism, and inhibit angiogenesis. There is an evidence that soy isoflavones may act on androgen receptors to inhibit tyrosine kinase activity, thereby blocking the growth and proliferation of cancer cells. Isoflavones may not significantly contribute to the hypolipidemic effects of soy protein, but may exert coronary benefits by improving endothelial function; in clinical trials of postmenopausal women, isoflavones improved flow-mediated dilation in women with impaired endothelial function. Some observational data suggests that isoflavones improve endothelial function by increasing the number of circulating endothelial progenitor cells, which replace damaged endothelial cells. Isoflavone may modulate the key transcription factors involved in the regulation of lipid metabolism by acting on the peroxisome proliferator-activated receptors (PPAR) alpha and gamma, which are receptors that regulate the transcription of genes involved in lipid and glucose homeostasis and lipid metabolism. Multiple biological actions of isoflavones, such as favorable effect on the blood lipid profile and inhibition of LDL cholesterol oxidation, may lead to cardio protective effects. [DB01645] has been shown to have antioxidant properties on hydrogen peroxide production _in vitro_ and blocks the formation of oxygen free radicals. Studies also suggest that at micromolar concentrations, genistein increases glucose-stimulated insulin secretion in cell lines and mouse pancreatic islets via a cAMP-dependent protein kinase mechanism. Based on the findings of experimental studies, genistein may exert a positive effect on bone formation by decreasing osteoclastic resorption factor, such as collagen C-telopeptide, and increasing osteoblastic formation markers, such as bone-alkaline phosphatase. _In vitro_, it antagonized the catabolic effects of parathyroid hormone (PTH) in osteoblasts by reversing the PTH-induced increase in soluble receptor activator of nuclear factor-xB ligand and decrease in osteoprotegerin expression.

Pharmacodynamics

Isolated soy protein with isoflavones was shown to decrease LDL cholesterol levels in randomized trials assessed by the American Heart Association. In a study of postmenopausal women, daily dietary intake of 101 mg of aglycone isoflavones (indicating [DB01645] and [DB13182]) was associated with lowered LDL cholesterol and apolipoprotein B levels by 8% and reduced systolic and diastolic blood pressure by 6.8% in hypertensive women. In a meta-analysis of randomized controlled trials of menopausal women, soy isoflavones attenuated bone loss of the spine and decreased the levels of deoxypyridinoline, a bone resorption marker, while increasing serum bone-specific alkaline phosphatase, a bone formation marker. The findings from studies investigating the effects of soy consumption on menopausal symptoms, breast cancer, and prostate cancer remain somewhat controversial and inconclusive. Consumption of soy isoflavones may decrease the markers of cancer development and progression in prostate cells, including prostate-specific antigen (PSA), testosterone, and androgen receptor in patients with prostate cancer but not in normal subjects. Although epidemiologic data in Asian women demonstrate that high soy food intake is associated with protection against breast cancer, soy foods have little effect on intermediary markers of breast cancer risk and postmenopausal soy intake may not reduce the risk of developing breast cancer. However, preliminary studies show that soy food intake reduces tumor recurrence in breast cancer patients. Soy isoflavones reported to interfere with thyroid peroxidase, which are involved in the production of thyroid hormones.

Mechanism of action

The exact mechanism of action of eugenol is unknown. However, eugenol has been shown to interrupt action potentials, which may be involved in its anti-pain activity. Research has also shown eugenol to have anti-inflammatory, neuroprotective, antipyretic, antioxidant, antifungal and analgesic properties. ... Thymocyte suspension was irradiated by gamma-rays, and the malondialdehyde (MDA) formation was measured with the thiobarbituric acid reactive species (TBARS) method. The results showed an increase in MDA in irradiated (2 Gy) thymocytes, which was inhibited in samples treated with increasing concentrations of eugenol (10-200 uM) prior to irradiation. The concentration of eugenol required to inhibit half of the MDA formation (IC(50)) in irradiated thymocytes was 100 uM. A dose-dependent increase in the generation of ROS was observed in irradiated thymocytes (0.5-200 cGy) as measured by 2,7-dichlorodihydro fluorescein diacetate (DCH-FDA), which was inhibited by eugenol administered before irradiation. Respiratory inhibition of isolated rat liver mitochondria by eugenol was dose related and uncoupled oxidative phosphorylation from electron transfer. Polymorphonuclear leukocytes (PMNL) play an important role in the modulation of inflammatory conditions in humans. PMNL cells recruited at the site of inflammation, release inflammatory mediators such as leukotrienes, proteolytic enzymes and reactive oxygen species. Among these, leukotrienes are implicated in pathophysiology of allergic and inflammatory disorders like asthma, allergic rhinitis, arthritis, inflammatory bowel disease and psoriasis. 5-lipoxygenase (5-LO) is the key enzyme in biosynthetic pathway of leukotrienes. Our earlier studies showed that spice phenolic active principles significantly inhibit 5-LO enzyme in human PMNLs. In this study we have further characterized the inhibitory mechanism of eugenol, the active principle of spice-clove on 5-LO enzyme and also its effect on leukotriene C((4)) (LTC(4)). Substrate dependent enzyme kinetics showed that the inhibitory effect of eugenol on 5-LO was of a non-competitive nature. Further, eugenol was found to significantly inhibit the formation of LTC(4) in calcium ionophore A23187 and arachidonic acid (AA) stimulated PMNL cells. These data clearly suggest that eugenol inhibits 5-LO by non-competitive mechanism and also inhibits formation of LTC(4) in human PMNL cells and thus may have beneficial role in modulating 5-LO pathway in human PMNL cells. The Ca(2+)-activated Cl(-) channel TMEM16A is involved in epithelial fluid secretion, smooth muscle contraction and neurosensory signaling. We identified a Thai herbal antidiarrheal formulation that inhibited TMEM16A Cl(-) conductance. C18-reversed-phase HPLC fractionation of the herbal formulation revealed >98% of TMEM16A inhibition activity in one out of approximately 20 distinct peaks. The purified, active compound was identified as eugenol (4-allyl-2-methoxyphenol), the major component of clove oil. Eugenol fully inhibited TMEM16A Cl(-) conductance with single-site IC(50)~150 uM. Eugenol inhibition of TMEM16A in interstitial cells of Cajal produced strong inhibition of intestinal contraction in mouse ileal segments. TMEM16A Cl(-) channel inhibition adds to the list of eugenol molecular targets and may account for some of its biological activities. For more Mechanism of Action (Complete) data for EUGENOL (21 total), please visit the HSDB record page.