VIGOR NMN FORMALLY DR VIGOR NMN 12000 CAPSULES (Each serving of 2 capsules contains B-nicotinamide mononucleotide/Pyrroloquinoline quinine disodium salt 200mg/10mg)

Indications

• Severe falciparum malaria
• Chloroquine-resistant malaria
• Malaria prophylaxis in high-risk areas

Dosage

Children: Child (body-weight 45 kg and above): Loading dose 20 mg

Adults: Loading dose: 20 mg/kg (max. 1.4 g) infused over 4 hours. Maintenance: 10 mg/kg every 8 hours (max. per dose 700 mg). For non-falciparum malaria, 600 mg every 8 hours for 5–7 days, in combination with doxycycline or clindamycin.

Mechanism of action

Quinine and related antimalarial drugs are theorized to be toxic to malaria parasites by interfering with their ability to digest hemoglobin. This leads to starvation of the parasite and accumulation of toxic levels of partially degraded hemoglobin. Quinine acts as a blood schizonticide and has been shown to inhibit heme polymerase, resulting in increased levels of cytotoxic heme within the parasite.

Pharmacodynamics

Quinine is particularly effective against chloroquine-resistant strains of Plasmodium falciparum. It acts as a blood schizonticide and possesses gametocytocidal activity against Plasmodium vivax and Plasmodium malariae. It is a weak base and becomes concentrated in the food vacuoles of the parasite, which enhances its antimalarial efficacy. Due to its side effects and toxicity, its use is generally reserved for severe cases of malaria.

Pharmacokinetics

Quinine is administered intravenously or orally, with a half-life that can vary based on the route of administration and the patient's renal function. Peak plasma concentrations are typically achieved within 1 to 3 hours of intravenous administration. It is metabolized in the liver and excreted primarily through urine. Dosing must be adjusted in cases of renal impairment to avoid toxicity.

Adverse effects

• alopecia
• angioedema
• bone marrow disorders
• choleostasis
• constipation
• diarrhoea
• fever
• gastric disorders
• megaloblastic anaemia
• oral disorders
• skin reactions
• vasculitis

Interactions

• quinine + digoxin: Moderate (increases concentration)
• hiv-protease inhibitors + quinine: Unknown (affects exposure)
• cimetidine + quinine: Unknown (increases exposure)
• rifampicin + quinine: Unknown (decreases exposure)

Precautions

• history of seizures-avoid large loading doses
• predisposition to folate deficiency

Pregnancy

Benefit of prophylaxis in malaria outweighs risk. Adequate folate supplements should be given to the mother.

Breast-feeding

Quinine is excreted in breast milk, caution is advised.

Storage

Store in a cool, dry place. Protect from light.

Formulations

• Quinine hydrochloride
• Quinine dihydrochloride
• Quinine sulfate

Indications

• Electrolyte replacement
• Volume expansion in hypovolemic patients
• Management of hyponatremia
• Support in intravenous fluid therapy

Dosage

Children: Refer to the BNF for Children for appropriate dosing in paediatric patients, as dosages may vary based on the formulation and clinical condition.

Adults: Refer to specific product information or clinical guidelines for dosage recommendations, as disodium is often part of combination products.

Mechanism of action

Disodium compounds often function by providing sodium ions that are essential for various physiological processes. Sodium ions play a critical role in maintaining osmotic balance, nerve impulse transmission, and muscle contraction. In the context of intravenous solutions, disodium helps to restore electrolyte balance in patients.

Pharmacodynamics

The pharmacodynamics of disodium is primarily related to its role in electrolyte balance and fluid homeostasis. Sodium ions are vital for the function of excitable tissues, including neurons and muscle cells. Changes in sodium levels can affect blood pressure, hydration status, and overall cellular function.

Pharmacokinetics

The pharmacokinetics of disodium compounds depend on their specific formulation and route of administration. When administered intravenously, disodium is rapidly distributed in the extracellular fluid, where it helps to maintain osmotic pressure. Sodium is primarily excreted by the kidneys, and its levels can be influenced by fluid intake, dietary sodium, and renal function.

Pregnancy

Use with caution. Consult a healthcare provider for specific guidance.

Breast-feeding

Use with caution. Consult a healthcare provider for specific guidance.

Storage

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

Indications

• Nutritional supplementation
• Support for cellular energy metabolism
• Potential adjunct in conditions requiring enhanced nucleic acid synthesis

Dosage

Children: Refer to established guidelines for specific dosing as it can vary based on the purpose of use and formulation.

Adults: Refer to established guidelines for specific dosing as it can vary based on the purpose of use and formulation.

Mechanism of action

Mononucleotide acts primarily as a substrate for the synthesis of nucleic acids. It participates in cellular energy metabolism through its role in the synthesis of ATP (adenosine triphosphate), which is the primary energy carrier in cells. Additionally, mononucleotides may influence signaling pathways within cells, particularly those related to growth and differentiation.

Pharmacodynamics

Mononucleotide exhibits effects related to energy metabolism and nucleic acid synthesis. By serving as a precursor for ATP and nucleic acids, it supports cellular functions and can influence cellular proliferation and repair mechanisms. The pharmacodynamic effects are influenced by the concentration of mononucleotide within the cellular environment and its availability for enzymatic reactions.

Pharmacokinetics

Mononucleotide absorption and metabolism can vary based on the specific type of mononucleotide and the route of administration. Generally, it is readily absorbed in the gastrointestinal tract when taken orally. Once in the bloodstream, it is distributed to tissues where it is either utilized for energy production or incorporated into nucleic acids. The elimination of mononucleotides is primarily through renal excretion, with some metabolites also being excreted in urine.

Adverse effects

• Gastrointestinal upset
• Headache
• Fatigue
• Dizziness

Precautions

• Use with caution in patients with renal impairment
• Monitor for potential side effects in patients with a history of gastrointestinal disorders

Pregnancy

Limited data available; consult healthcare provider before use.

Breast-feeding

Limited data available; consult healthcare provider before use.

Storage

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

Formulations

• Oral tablets
• Powder for reconstitution

Mechanism of action

Pyrroloquinoline functions primarily as a cofactor for various enzymatic reactions. It has been shown to participate in redox reactions, facilitating electron transfer processes, which can enhance cellular energy production and reduce oxidative stress. This mechanism is critical in various metabolic pathways, including those involved in amino acid and carbohydrate metabolism.

Pharmacodynamics

Pyrroloquinoline exhibits antioxidant activity, which helps to mitigate oxidative stress in cells. This action can protect cellular components from damage caused by reactive oxygen species (ROS). Additionally, it may influence signal transduction pathways associated with cell survival and growth, thereby playing a role in various physiological processes.

Pharmacokinetics

The pharmacokinetics of pyrroloquinoline, including its absorption, distribution, metabolism, and excretion, are not well characterized in the literature. More research is needed to fully understand how this compound behaves in the human body, including its bioavailability and half-life.

Pregnancy

There is insufficient data on the safety of pyrroloquinoline during pregnancy. Caution is advised.

Breast-feeding

Insufficient data on excretion in human milk. Caution is advised.

Storage

Store at room temperature, away from light and moisture.

Indications

• Fluid and electrolyte replenishment
• Management of hyponatremia
• Induction of abortion in specific medical circumstances

Dosage

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

Adults: Refer to the BNF for specific dosing guidelines based on clinical context and condition being treated.

Mechanism of action

Sodium and chloride, as major electrolytes in the extracellular fluid, work together to control extracellular volume and blood pressure. Disturbances in sodium concentrations are linked to disorders of water balance. Intra-amniotic instillation of hypertonic sodium chloride may induce uterine contractions, leading to abortion, potentially mediated by prostaglandins released from damaged decidual cells.

Pharmacodynamics

Sodium, the principal cation in extracellular fluid, is critical for regulating water distribution, fluid balance, and osmotic pressure in body fluids. It works in conjunction with chloride and bicarbonate to maintain acid-base equilibrium. Chloride, as the major extracellular anion, mirrors sodium metabolism, and alterations in acid-base balance are reflected in chloride concentrations.

Pharmacokinetics

Sodium and chloride ions are absorbed from the gastrointestinal tract and distributed throughout the body fluids. Their concentration in extracellular fluid is tightly regulated by mechanisms involving renal excretion and hormonal control, primarily through aldosterone. Changes in dietary intake can also influence sodium levels significantly.

Pregnancy

Intra-amniotic instillation of hypertonic sodium chloride is associated with abortion and fetal death. Caution is advised during pregnancy.

Breast-feeding

Sodium is considered safe during breastfeeding as it is an essential electrolyte.

Storage

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

Formulations

• 20% sodium chloride injection

Mechanism of action

The theorized mechanism of action for quinine and related anti-malarial drugs is that these drugs are toxic to the malaria parasite. Specifically, the drugs interfere with the parasite's ability to break down and digest hemoglobin. Consequently, the parasite starves and/or builds up toxic levels of partially degraded hemoglobin in itself. Quinine has a local anesthetic action and analgesic, antipyretic, and oxytocic effects. Quinine also has cardiovascular effects similar to those of quinidine.

Pharmacodynamics

Quinine is used parenterally to treat life-threatening infections caused by chloroquine-resistant Plasmodium falciparum malaria. Quinine acts as a blood schizonticide although it also has gametocytocidal activity against P. vivax and P. malariae. Because it is a weak base, it is concentrated in the food vacuoles of P. falciparum. It is thought to act by inhibiting heme polymerase, thereby allowing accumulation of its cytotoxic substrate, heme. As a schizonticidal drug, it is less effective and more toxic than chloroquine. However, it has a special place in the management of severe falciparum malaria in areas with known resistance to chloroquine.

Mechanism of action

Sodium and chloride - major electrolytes of the fluid compartment outside of cells (i.e., extracellular) - work together to control extracellular volume and blood pressure. Disturbances in sodium concentrations in the extracellular fluid are associated with disorders of water balance. Intra-amniotic instillation of 20% sodium chloride injection induces abortion and fetal death. Although the mechanism has not been conclusively determined, some studies indicate that the drug's abortifacient activity may be mediated by prostaglandins released from decidual cells damaged by hypertonic solutions of sodium chloride. Hypertonic sodium chloride-induced uterine contractions are usually sufficient to cause evacuation of both the fetus and placenta; however, abortion may be incomplete in 25-40% of patients. /20% injection/

Pharmacodynamics

Sodium, the major cation of the extracellular fluid, functions primarily in the control of water distribution, fluid balance, and osmotic pressure of body fluids. Sodium is also associated with chloride and bicarbonate in the regulation of the acid-base equilibrium of body fluid. Chloride, the major extracellular anion, closely follows the metabolism of sodium, and changes in the acid-base balance of the body are reflected by changes in the chloride concentration.