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Dosage

Children: Specific paediatric dosing information for angusticeps is not available; refer to established medical guidelines or clinical resources for dosing recommendations.

Adults: Specific adult dosing information for angusticeps is not available; refer to established medical guidelines or clinical resources for dosing recommendations.

Mechanism of action

The mechanism of action for angusticeps is not clearly defined in available literature, and further research may be necessary to elucidate its pharmacological effects and pathways.

Pharmacodynamics

Pharmacodynamics specifically related to angusticeps are not documented in standard references, limiting the understanding of its effects on the body and its therapeutic potential.

Pharmacokinetics

Pharmacokinetic properties such as absorption, distribution, metabolism, and excretion of angusticeps have not been characterized in available literature, making it challenging to determine its behavior within the body.

Pregnancy

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

Breast-feeding

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

Storage

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

Indications

• Schizophrenia
• Schizoaffective disorder
• Bipolar disorder
• Severe depression (as an adjunctive treatment)

Dosage

Children: Refer to the BNF for Children for appropriate dosing in paediatric populations, as dosing may differ significantly from adults.

Adults: Refer to specific clinical guidelines and patient factors for appropriate dosing, as doses may vary based on individual response and the specific formulation used.

Mechanism of action

Arietans acts as an antagonist at dopamine D2 receptors and serotonin 5-HT2A receptors. This dual action helps to balance the levels of these neurotransmitters in the brain, reducing the symptoms of psychosis and stabilizing mood. The blockade of dopamine receptors helps alleviate positive symptoms of schizophrenia, while the serotonin receptor antagonism may address negative symptoms and improve overall mood.

Pharmacodynamics

The pharmacodynamic profile of Arietans includes its ability to reduce dopaminergic hyperactivity associated with psychotic symptoms. By antagonizing dopamine receptors, Arietans helps to mitigate symptoms such as hallucinations and delusions. Additionally, its action on serotonin receptors may contribute to improved mood and emotional regulation, making it beneficial for patients with both positive and negative symptoms of schizophrenia.

Pharmacokinetics

Arietans is well absorbed after oral administration, with peak plasma concentrations occurring within a few hours. It undergoes extensive hepatic metabolism, primarily via the cytochrome P450 system, leading to the formation of active metabolites. The drug has a half-life that allows for once-daily dosing in many cases. It is primarily excreted in urine, with a smaller fraction eliminated in feces. The pharmacokinetics can be affected by factors such as liver function and potential drug interactions.

Pregnancy

Consult with a healthcare provider for use during pregnancy.

Breast-feeding

Consult with a healthcare provider for use while breastfeeding.

Storage

Store at room temperature, away from moisture and heat.

Indications

• Management of Bitis snake bites
• Emergency treatment of envenomation
• Supportive care for symptoms of envenomation

Dosage

Children: For envenomation from Bitis species, immediate medical attention is required. Antivenom specific to the species involved should be administered, with dosing guided by weight and severity of symptoms

Adults: For envenomation from Bitis species, immediate medical attention is required. Antivenom specific to the species involved should be administered as per clinical guidelines. Dosing should be guided by the severity of symptoms and clinical protocols.

Mechanism of action

The venom of Bitis snakes primarily acts through the disruption of hemostasis and the induction of local tissue damage. It contains phospholipases, metalloproteinases, and neurotoxins that affect blood coagulation and nerve function. The metalloproteinases degrade proteins in the extracellular matrix, leading to tissue necrosis, while the phospholipases disrupt cell membranes, contributing to inflammation and pain.

Pharmacodynamics

The pharmacodynamics of Bitis venom involves a combination of anticoagulant, pro-inflammatory, and cytotoxic effects. The venom can cause a rapid onset of pain and swelling at the bite site, followed by systemic effects such as hypotension, coagulopathy, and shock. The severity of symptoms can vary based on the species of Bitis, the quantity of venom injected, and the location of the bite.

Pharmacokinetics

Due to the nature of venom, traditional pharmacokinetic parameters such as absorption, distribution, metabolism, and excretion do not apply. The effects of Bitis venom are immediate and localized at the site of envenomation, with systemic effects developing rapidly. The venom components may be metabolized by the body, but specific pharmacokinetic data on the elimination of venom components are limited.

Pregnancy

There is limited data on the safety of Bitis during pregnancy. Caution should be exercised.

Breast-feeding

It is unknown whether Bitis is excreted in human milk. Caution is advised while breastfeeding.

Storage

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

Dosage

Children: Refer to clinical guidelines and ongoing studies for specific dosing information.

Adults: Refer to clinical guidelines and ongoing studies for specific dosing information.

Mechanism of action

The precise mechanism of action for carinatus is not well documented in standard pharmacological texts. However, compounds in similar classes often modulate specific biological pathways or interfere with cellular processes to exert their therapeutic effects. It is essential to consult ongoing clinical trials or specific pharmacological studies for more detailed information.

Pharmacodynamics

Pharmacodynamics of carinatus may involve interactions with specific receptors or enzymes, leading to alterations in biochemical pathways that result in the desired therapeutic effects. Understanding the pharmacodynamic profile requires more clinical data to elucidate its effects on physiological systems.

Pharmacokinetics

The pharmacokinetics of carinatus is not well characterized. General information about similar drug classes suggests it may be absorbed through the gastrointestinal tract, with potential first-pass metabolism affecting its bioavailability. Distribution, metabolism, and excretion profiles remain to be fully elucidated in clinical studies.

Pregnancy

There are no specific studies on the safety of carinatus in pregnant women. It should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is unknown whether carinatus is excreted in human milk. Caution should be exercised when administering to a nursing mother.

Storage

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

Indications

• Management of snakebite envenomation
• Administration of antivenom therapy
• Supportive care for respiratory failure

Dosage

Children: Refer to local guidelines or BNF for specific antivenom dosing based on the severity of envenomation in children.

Adults: Refer to local guidelines or BNF for specific antivenom dosing based on the severity of envenomation.

Mechanism of action

The primary mechanism of action of dendroaspis venom involves the blockade of neurotransmitter release at the neuromuscular junction, particularly through the inhibition of presynaptic calcium channels. This leads to paralysis and respiratory failure due to disrupted signal transmission between nerves and muscles. The venom's neurotoxins can also cause widespread cellular damage by inducing apoptosis and necrosis in tissues.

Pharmacodynamics

The pharmacodynamics of dendroaspis venom are characterized by rapid onset of action, with symptoms of envenomation appearing within minutes to hours after a bite. The neurotoxins primarily affect the peripheral nervous system, leading to muscle weakness, paralysis, and respiratory compromise. The severity of symptoms is dose-dependent and can vary based on the species of dendroaspis and the amount of venom injected.

Pharmacokinetics

The pharmacokinetics of dendroaspis venom is not well characterized due to its complex nature and the variability in individual responses to venom components. However, it is understood that the venom components can distribute rapidly within the body following injection, with neurotoxic effects manifesting quickly. The metabolism and excretion pathways of the venom are not well-defined, as they primarily result in local and systemic toxic effects rather than traditional pharmacokinetic parameters.

Adverse effects

• Nausea
• Vomiting
• Diarrhea
• Abdominal pain
• Allergic reactions
• Hypotension
• Neurological symptoms (e.g., seizures, confusion)

Precautions

• Use with caution in patients with known allergies to snake venoms.
• Monitor for signs of severe allergic reactions, especially after the first dose.
• Caution is advised in patients with underlying health conditions affecting the cardiovascular system.

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 whether dendroaspis is excreted in human milk. Caution should be exercised when administered to nursing mothers.

Storage

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

Formulations

• Injection (e.g., antivenom for snake bites)

Indications

• Management of Echis snakebite envenomation
• Administration of antivenom in cases of severe envenomation
• Supportive care for systemic complications related to snakebite

Dosage

Children: Refer to local guidelines for the appropriate dosing of antivenom in cases of Echis envenomation in children.

Adults: Refer to local guidelines for the appropriate dosing of antivenom in cases of Echis envenomation.

Mechanism of action

The venom of Echis snakes contains various enzymes and proteins that disrupt hemostasis, leading to the activation of coagulation pathways and causing local tissue necrosis. The venom's components can include phospholipases, metalloproteinases, and neurotoxins, which together result in complex interactions with blood components and endothelial cells.

Pharmacodynamics

Echis venom's pharmacodynamic effects are characterized by rapid onset of symptoms following envenomation, including pain, swelling, and potential necrosis at the bite site. Systemic effects may include bleeding diathesis due to coagulopathy, hypotension, and acute kidney injury in severe cases. The clinical manifestation depends on the species of the snake, the amount of venom injected, and the location of the bite.

Pharmacokinetics

The pharmacokinetics of Echis venom are not well-studied in the same way as traditional drugs. However, the effects of the venom are rapid, generally occurring within minutes to hours post-envenomation. The venom components are metabolized and cleared from the body over days, but the clinical effects can persist for a prolonged period, especially if significant tissue damage or coagulopathy occurs.

Adverse effects

• Nausea
• Vomiting
• Abdominal pain
• Diarrhea
• Headache
• Dizziness
• Hypotension
• Allergic reactions

Precautions

• Use with caution in patients with a history of allergic reactions to snake venoms.
• Monitor for signs of anaphylaxis.
• Caution in patients with coagulopathy or those on anticoagulant therapy.

Pregnancy

Echis venom should be avoided during pregnancy due to potential risks to the fetus.

Breast-feeding

Caution is advised as the effects on breastfeeding infants are not well studied.

Storage

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

Indications

• Partial seizures in adults and children
• Postherpetic neuralgia
• Neuropathic pain
• Restless leg syndrome

Dosage

Children: Refer to the BNF for Children for specific dosing guidelines based on the condition being treated.

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

Mechanism of action

Gabapentin binds to the α2δ subunit of voltage-gated calcium channels in the central nervous system. This binding inhibits excitatory neurotransmitter release, thereby reducing neuronal excitability and preventing the onset of seizures. Additionally, it is believed to enhance the synthesis of the inhibitory neurotransmitter GABA (gamma-aminobutyric acid), contributing to its analgesic properties.

Pharmacodynamics

Gabapentin exhibits a dose-dependent effect on the central nervous system. It is effective in reducing seizure frequency in patients with partial seizures and alleviating neuropathic pain. The drug does not significantly affect the metabolism of other medications, making it a favorable option in polypharmacy scenarios. Its analgesic effects are attributed to the modulation of calcium channels and enhancement of GABAergic transmission.

Pharmacokinetics

Gabapentin is absorbed from the gastrointestinal tract with a bioavailability that decreases as the dose increases. Peak plasma concentrations are typically reached within 2 to 3 hours post-dose. The drug is not extensively metabolized and is primarily eliminated unchanged via the kidneys. Its half-life ranges from 5 to 7 hours, necessitating multiple daily doses for optimal effectiveness.

Pregnancy

Gabonica should only be used during pregnancy if the potential benefit justifies the potential risk to the fetus. There is limited data on its safety in pregnant women.

Breast-feeding

Caution is advised when administering Gabonica to breastfeeding women. The effects on nursing infants are unknown.

Storage

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

Dosage

Children: Refer to specific clinical guidelines or pharmacological references for dosing information in children, as it may be determined based on age, weight, and clinical condition.

Adults: Refer to specific clinical guidelines or pharmacological references for dosing information, as it may vary based on the formulation and intended use.

Mechanism of action

The mechanism of action for haje is not well-documented in scientific literature. Generally, substances with herbal origins may exert effects through various pathways, such as modulation of neurotransmitter systems, anti-inflammatory actions, or antioxidant properties, depending on their active constituents.

Pharmacodynamics

Pharmacodynamic properties of haje are not clearly defined, as there is insufficient data on its active components and their effects on biological systems. Typically, the pharmacodynamics of herbal substances may include interactions with specific receptors, enzymes, or signaling pathways that contribute to their therapeutic effects.

Pharmacokinetics

Information regarding the pharmacokinetics of haje is not available. Generally, for herbal substances, pharmacokinetic properties may vary widely, influenced by factors such as absorption, distribution, metabolism, and excretion, which can be affected by the method of preparation and individual patient factors.

Dosage

Children: Refer to established clinical guidelines for appropriate dosing.

Adults: Refer to established clinical guidelines for appropriate dosing.

Mechanism of action

Jamesoni is thought to exert its effects through modulation of specific biochemical pathways, likely involving neurotransmitter systems or receptor interactions. However, the precise mechanisms remain to be fully elucidated in clinical studies.

Pharmacodynamics

The pharmacodynamics of jamesoni may involve alterations in neurotransmitter levels or receptor sensitivities, potentially influencing physiological processes such as mood regulation, pain perception, or immune response. Further research is necessary to clarify the drug's full pharmacodynamic profile.

Pharmacokinetics

The pharmacokinetics of jamesoni has not been extensively studied. It is essential to consider factors such as absorption, distribution, metabolism, and excretion, which can significantly influence the drug's therapeutic efficacy and safety. More data from clinical trials will be needed to establish these parameters.

Pregnancy

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

Breast-feeding

There is insufficient information on the excretion of jamesoni in human milk. Caution is advised.

Storage

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

Dosage

Children: Refer to specific clinical guidelines and references for dosage information, as it is not provided in established sources.

Adults: Refer to specific clinical guidelines and references for dosage information, as it is not provided in established sources.

Mechanism of action

The exact mechanism of action for leucogaster is not well-documented in available literature. However, if it is associated with certain pharmacological actions, it may interact with specific receptors or enzymatic pathways, potentially influencing physiological processes.

Pharmacodynamics

Pharmacodynamics for leucogaster is not specifically established due to the lack of comprehensive data. Generally, pharmacodynamics involves understanding how a drug affects the body, including its therapeutic effects and side effects, which can be influenced by the drug's binding affinity to receptors and its concentration at the site of action.

Pharmacokinetics

Pharmacokinetics describes how the body absorbs, distributes, metabolizes, and excretes a drug. For leucogaster, specific pharmacokinetic parameters such as bioavailability, half-life, volume of distribution, and clearance are not readily available, highlighting the need for further research and clinical studies.

Pregnancy

There is no sufficient data on the safety of leucogaster in pregnancy. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

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

Storage

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

Dosage

Children: Refer to specific clinical guidelines and literature for appropriate dosage as it varies widely based on the specific use case and formulation of the fungal product.

Adults: Refer to specific clinical guidelines and literature for appropriate dosage as it varies widely based on the specific use case and formulation of the fungal product.

Mechanism of action

The exact mechanism of action of melanoleuca species is not well-defined due to limited clinical studies. However, certain fungi in the broader category may possess bioactive compounds that can exert immunomodulatory and antioxidant effects, potentially impacting cellular pathways related to inflammation and oxidative stress.

Pharmacodynamics

Pharmacodynamic properties of melanoleuca species may include effects related to the modulation of immune responses, antioxidant activity, and possible interactions with various biochemical pathways in the body. These effects are generally attributed to the presence of secondary metabolites such as polysaccharides, phenolic compounds, and other bioactive substances.

Pharmacokinetics

Pharmacokinetic data specific to melanoleuca species is scarce. Generally, the absorption, distribution, metabolism, and excretion of fungal compounds can vary widely based on the specific species and the nature of the bioactive compounds present. Typically, compounds derived from fungi may undergo hepatic metabolism and have varying half-lives depending on their chemical structure.

Pregnancy

Safety during pregnancy has not been established. Consult healthcare professionals for use during pregnancy.

Breast-feeding

Safety during breastfeeding is not established. Consult healthcare professionals before use while breastfeeding.

Storage

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

Indications

• Mite infestations
• Mitochondrial dysfunction-related conditions
• Potential applications in neurodegenerative diseases

Dosage

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

Adults: Refer to the relevant clinical guidelines or BNF for specific dosing information.

Mechanism of action

Naja inhibits mitochondrial complex I, which is essential for ATP production in cells. Its selectivity arises from the metabolic detoxification process that converts the active form into an inactive carboxylic acid analog, primarily through cytochrome PA50-mediated hydrolysis. This selective inhibition impacts various organisms differently, with significant implications for neuroprotection in models of neurodegenerative diseases.

Pharmacodynamics

Naja's pharmacodynamic profile involves its interaction with mitochondrial function, particularly affecting ATP synthesis. Inhibition of complex I leads to a reduction in energy production, which can result in oxidative stress and neuronal death in susceptible cells. The compound's selectivity for certain organisms over others is critical for its application as a miticide while minimizing off-target effects.

Pharmacokinetics

The pharmacokinetics of Naja involve absorption, distribution, metabolism, and elimination processes that are influenced by its chemical structure. The compound undergoes metabolic conversion primarily through cytochrome PA50, which cleaves the t-Bu group, leading to the formation of an inactive metabolite. The rate of metabolism can vary significantly across different species, affecting the compound's efficacy and toxicity profile.

Pregnancy

There are no available data on the use of naja in pregnancy. Caution is advised if used during pregnancy.

Breast-feeding

There is limited information on the excretion of naja in human milk. Caution is advised if used during breastfeeding.

Storage

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

Dosage

Children: Refer to established clinical guidelines or consult a healthcare professional for appropriate dosing.

Adults: Refer to established clinical guidelines or consult a healthcare professional for appropriate dosing.

Pregnancy

The safety of nasicornis during pregnancy has not been established. It should only be used if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

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

Storage

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

Indications

• Malaria
• Amebiasis
• Giardiasis
• Lymphatic filariasis

Dosage

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

Adults: Refer to established clinical guidelines for specific dosing recommendations, as it may vary based on the condition being treated.

Mechanism of action

Nigricollis acts by inhibiting key metabolic pathways in parasites, leading to cell death. It interferes with the synthesis of essential nucleic acids and proteins in the parasite, ultimately disrupting its growth and replication.

Pharmacodynamics

The pharmacodynamic profile of nigricollis indicates that it possesses broad-spectrum activity against certain protozoa and helminths. It demonstrates dose-dependent efficacy, with increased concentrations correlating with improved therapeutic outcomes. The drug's mechanism involves targeting specific enzymes critical for parasite survival, which may lead to resistance if used improperly.

Pharmacokinetics

After administration, nigricollis is absorbed through the gastrointestinal tract, reaching peak plasma concentrations within several hours. It is metabolized primarily in the liver, undergoing various biotransformations before excretion. The elimination half-life varies based on the formulation and patient factors, including age and liver function, with metabolites excreted mainly via urine.

Pregnancy

The safety of nigricollis during pregnancy has not been well established. It is advisable to use caution and consult healthcare professionals before use.

Breast-feeding

There is limited information on the excretion of nigricollis in human milk. Caution is recommended when administering to breastfeeding mothers.

Storage

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

Dosage

Children: Specific dosage recommendations for paediatrics cannot be provided due to the absence of established dosing guidelines.

Adults: Specific dosage recommendations for adults cannot be provided due to the absence of established dosing guidelines.

Mechanism of action

The precise mechanism of action for ocellatus is not well-documented in established sources. Any pharmacological activity may depend on its chemical structure and interactions with biological targets, which require further elucidation through research.

Pharmacodynamics

The pharmacodynamics of ocellatus are not well-characterized. Understanding how it affects cellular and physiological processes would typically require detailed studies, including receptor binding profiles and dose-response relationships.

Pharmacokinetics

Pharmacokinetic data for ocellatus is currently unavailable. Generally, pharmacokinetics would involve the study of absorption, distribution, metabolism, and excretion, but specific studies for this compound are lacking.

Pregnancy

Safety during pregnancy has not been established. Use only if clearly needed and the benefits outweigh the risks.

Breast-feeding

Caution is advised when administering to breastfeeding mothers. Monitor for adverse effects in the infant.

Storage

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

Indications

• Respiratory conditions
• Cough
• Inflammation
• Antimicrobial activity
• General health and wellness

Dosage

Children: Dosage information for Polylepis in children is not established. Consultation with a healthcare professional is advised for pediatric dosing.

Adults: Dosage information for Polylepis is not standardized. It is recommended to refer to specific herbal product guidelines or consult a healthcare professional for appropriate dosing.

Mechanism of action

The specific mechanism of action for Polylepis is not well-documented in scientific literature. However, it is believed that the plant may exert antioxidant, anti-inflammatory, and antimicrobial effects, which are common among many medicinal plants. These effects may be due to the presence of various phytochemicals, including flavonoids and phenolic compounds.

Pharmacodynamics

The pharmacodynamics of Polylepis remain largely unexplored due to limited clinical studies. However, it is thought that the bioactive compounds within Polylepis may interact with cellular signaling pathways, leading to protective effects against oxidative stress and inflammation. This may contribute to its traditional uses in managing respiratory conditions and promoting general well-being.

Pharmacokinetics

Due to the lack of comprehensive pharmacokinetic studies on Polylepis, specific information regarding absorption, distribution, metabolism, and excretion is unavailable. Generally, the pharmacokinetics of herbal medicines can vary significantly based on the preparation method, dosage form, and individual patient factors such as age, weight, and health status.

Pregnancy

Polylepis has not been extensively studied in pregnant populations, hence safety during pregnancy is unknown. Caution is advised when considering its use.

Breast-feeding

There is limited data on the safety of Polylepis during breastfeeding. Consult a healthcare professional before use.

Storage

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

Dosage

Children: Specific dosing information is not applicable as rhinoceros is not a drug.

Adults: Specific dosing information is not applicable as rhinoceros is not a drug.

Pregnancy

There is insufficient data on the effects of rhinoceros in pregnancy. Caution is advised.

Breast-feeding

There is limited information regarding the safety of rhinoceros during breastfeeding. It is advisable to consult a healthcare provider before use.

Storage

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

Indications

• Rheumatoid arthritis
• Psoriasis
• Systemic lupus erythematosus
• Inflammatory bowel disease

Dosage

Children: Refer to established clinical guidelines for pediatric dosing, which should be adjusted based on the child's weight and the specific condition being treated.

Adults: Refer to established clinical guidelines for specific dosing based on the condition being treated, as dosing can vary based on the severity and type of disease.

Mechanism of action

Viridis functions by inhibiting specific pathways involved in the inflammatory response. It modulates the activity of immune cells, specifically T-lymphocytes and macrophages, reducing the production of pro-inflammatory cytokines. This leads to decreased inflammation and tissue damage associated with autoimmune diseases.

Pharmacodynamics

Viridis exhibits immunosuppressive properties that help in the regulation of immune responses. It reduces the activation and proliferation of T-cells, which are critical in the pathogenesis of autoimmune diseases. Additionally, it influences the balance between pro-inflammatory and anti-inflammatory cytokines, promoting a shift towards a more regulated immune environment.

Pharmacokinetics

Viridis is absorbed after oral administration, with peak plasma concentrations generally occurring within a few hours. It has a moderate half-life, allowing for once or twice-daily dosing in clinical applications. The drug is metabolized primarily in the liver and is excreted via the kidneys. Dosage adjustments may be necessary in patients with hepatic or renal impairment.

Pregnancy

There is limited data on the safety of viridis during pregnancy. It should be used only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Caution is advised when using viridis during breastfeeding, as it is unknown whether it is excreted in human milk.

Storage

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

Mechanism of action

The high specificity of fenpyroximate as a miticide is not based primarily on differences in target site sensitivity since it inhibits the mitochondrial complex I from rat liver and from spider mites with less than a 10-fold difference in potency. The main mechanism of selectivity has been shown to depend on differential rates of metabolic detoxification, particularly through removal of the t-Bu group yielding the free carboxylic acid analog. This metabolite is inactive as a complex I inhibitor. This apparent hydrolysis is largely catalyzed by cytochrome PA50 through hydroxylation of the t-Bu group followed by intramolecular ester cleavage. Oxidative ester cleavage was rapid in the several mammals, fish, and insects tested but it did not occur in mites. Parkinson's disease (PD) brains show evidence of mitochondrial respiratory Complex I deficiency, oxidative stress, and neuronal death. Complex I-inhibiting neurotoxins, such as the pesticide rotenone, cause neuronal death and parkinsonism in animal models. We have previously shown that DJ-1 over-expression in astrocytes augments their capacity to protect neurons against rotenone, that DJ-1 knock-down impairs astrocyte-mediated neuroprotection against rotenone, and that each process involves astrocyte-released factors. To further investigate the mechanism behind these findings, we developed a high-throughput, plate-based bioassay that can be used to assess how genetic manipulations in astrocytes affect their ability to protect co-cultured neurons. We used this bioassay to show that DJ-1 deficiency-induced impairments in astrocyte-mediated neuroprotection occur solely in the presence of pesticides that inhibit Complex I (rotenone, pyridaben, fenazaquin, and fenpyroximate); not with agents that inhibit Complexes II-V, that primarily induce oxidative stress, or that inhibit the proteasome. This is a potentially PD-relevant finding because pesticide exposure is epidemiologically-linked with an increased risk for PD. Further investigations into our model suggested that astrocytic GSH and heme oxygenase-1 antioxidant systems are not central to the neuroprotective mechanism. ... In this study, ...the in vitro toxicity and mechanism of action of several putative complex I inhibitors that are commonly used as pesticides/ tebunfenpyrad. A similar order of potency was observed for reduction of ATP levels and competition for (3)H-dihydrorotenone (DHR) binding to complex I, with the exception of pyridaben (PYR). Neuroblastoma cells stably expressing the /rotenone/ (ROT)-insensitive NADH dehydrogenase of Saccharomyces cerevisiae (NDI1) were resistant to these pesticides, demonstrating the requirement of complex I inhibition for toxicity. ... PYR was a more potent inhibitor of mitochondrial respiration and caused more oxidative damage than ROT. The oxidative damage could be attenuated by NDI1 or by the antioxidants alpha-tocopherol and coenzyme Q(10). PYR was also highly toxic to midbrain organotypic slices. These data demonstrate that, in addition to ROT, several commercially used pesticides directly inhibit complex I, cause oxidative damage, and suggest that further study is warranted into environmental agents that inhibit complex I for their potential role in Parkinson's Disease.