Ektoban

Indications

• Fungal infections
• Dermatophytosis
• Candidiasis
• Onychomycosis

Dosage

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

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

Mechanism of action

Cymiazole works by inhibiting the enzyme lanosterol 14α-demethylase, which is involved in the biosynthesis of ergosterol, a key component of the fungal cell membrane. This disruption in ergosterol synthesis leads to increased permeability of the cell membrane and ultimately results in cell lysis.

Pharmacodynamics

The pharmacodynamics of cymiazole involve its fungicidal activity against a variety of fungi. By targeting the ergosterol biosynthesis pathway, cymiazole alters the integrity of the fungal cell membrane, causing leakage of cellular contents and inhibiting fungal growth. The drug exhibits activity against dermatophytes, yeasts, and some filamentous fungi.

Pharmacokinetics

Cymiazole is absorbed following oral administration and distributed throughout the body. It has a moderate half-life, allowing for once or twice daily dosing in most cases. The drug undergoes hepatic metabolism and is excreted primarily via the urine. Its pharmacokinetic profile can vary based on individual patient factors, including age, liver function, and concurrent medications.

Pregnancy

The safety of cymiazole during pregnancy is not well established. It should be used only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Cymiazole is not recommended during breastfeeding due to insufficient data on excretion in human milk.

Storage

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

Indications

• Control of agricultural pests
• Public health pest control
• Vector control for diseases transmitted by insects

Dosage

Children: Refer to specific guidelines based on the formulation and target pest, as dosages can vary widely. Consult the product label or BNF for precise dosing information.

Adults: Refer to specific guidelines based on the formulation and target pest, as dosages can vary widely. Consult the product label or BNF for precise dosing information.

Mechanism of action

Cypermethrin exerts its effects primarily at voltage-sensitive sodium channels in both insect and mammalian neurons. It enhances the binding of specific ligands to these channels, leading to prolonged depolarization of the neuron and disruption of normal nerve function. Additionally, cypermethrin may also act on the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex, further contributing to its neurotoxic effects.

Pharmacodynamics

As a pyrethroid, cypermethrin has a high affinity for sodium channels, which causes sustained activation and subsequent paralysis of the insect’s nervous system. This mechanism results in the inability of the insect to coordinate movement or respond to stimuli, ultimately leading to death. The insecticidal potency is influenced by the stereochemistry of the compound, with different isomers demonstrating varying levels of effectiveness.

Pharmacokinetics

Cypermethrin is absorbed through the exoskeleton of insects and can also be absorbed through the skin in mammals. Once in the system, it is metabolized in the liver, with metabolites excreted primarily in urine. The compound has a relatively low bioavailability in mammals and is rapidly eliminated. Environmental factors such as temperature and moisture can influence its degradation and persistence in the environment.

Adverse effects

• Skin irritation
• Respiratory issues
• Nausea
• Headache
• Dizziness

Precautions

• Use with caution in patients with known hypersensitivity to pyrethroids
• Avoid contact with eyes and mucous membranes
• Use personal protective equipment when handling

Pregnancy

Cypermethrin should be used in pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether cypermethrin is excreted in human milk; caution should be exercised when administering to breastfeeding women.

Storage

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

Formulations

• Liquid concentrate
• Aerosol spray
• Emulsifiable concentrate

Mechanism of action

Pyrethroid insecticides are synthetic neurotoxins patterned after the naturally occurring pyrethrins. Their mechanism of action is thought to involve effects primarily at the voltage-sensitive sodium channel of both insect & mammalian neurons, although recent studies have raised the possibility that these cmpds may also act at the gamma-aminobutyric acid receptor-chloride ionophore complex. Here we show that active pyrethroids of the alpha-cyano-3-phenoxybenzyl class allosterically enhance the binding of (3)H-batrachotoxinin-A 20-alpha-benzoate to voltage-sensitive sodium channels of rat brain in a dose-dependent & stereospecific manner. Comparison of the rank order of potency for enhancement of (3)H-batrachotoxinin-A 20-alpha-benzoate binding & insecticidal activity in a series of toxic steroisomers of cypermethrin, representative of the class, reveals a correlation between the two measures. These results support a sodium channel site model for pyrethroid action & suggest a useful & practical method to help evaluate the relationship between the sodium channel & insecticidal potency for members of this class of cmpds. Following absorption through the chitinous exoskeleton of arthropods, pyrethrins stimulate the nervous system, apparently by competitively interfering with cationic conductances in the lipid layer of nerve cells, thereby blocking nerve impulse transmissions. Paralysis and death follow. /Pyrethrins/ The efforts of this study were directed at defining the importance of esterases, mixed function oxidases and mitochondrial respiratory chain enzymes in in vitro covalent binding of cismethrin and the two cyanopyrethroids, cypermethrin and deltamethrin to phenobarbital induced rat liver homogenate and microsomes. Each enzyme system was selectively inhibited to elucidate the activation mechanism involved. Piperonyl-butoxide and carbon-monoxide were used to inhibit mixed function oxidases. Tetraethylpyrophosphate inhibited esterase and trichloropropene-oxide inhibited epoxide-hydrolase. Potassium cyanide or rotenone was used to block the mitochondrial electron transport. The study demonstrated that covalent binding of cismethrin, cypermethrin, and deltamethrin was dependent on pyrethroid concentration. Inhibition of esterases and mitochondrial respiration only slightly altered the covalent binding level. Inhibition of cytochrome p450 and mixed function oxidases reduced the covalent binding, making it almost nonexistent. The covalent binding was decreased by 50% through an 80% inhibition of epoxide-hydrolase. In vitro, the comparison of data between alcohol and acid labeling of the same pyrethroid suggested that the whole molecule was bound to proteins in an activation process, perhaps epoxidation, and that hydrolysis could only occur afterwards. The role of cytochrome p450 dependent monooxygenases in the covalent binding process was stressed. Interaction with sodium channels is not the only mechanism of action proposed for the pyrethroids. Their effects on the CNS have led various workers to suggest actions via antagonism of gamma-aminobutyric acid (GABA)-mediated inhibition, modulation of nicotinic cholinergic transmission, enhancement of noradrenaline release, or actions on calcium ions. Since neurotransmitter specific pharmacological agents offer only poor or partial protection against poisoning, it is unlikely that one of these effects represents the primary mechanism of action of the pyrethroids, & most neurotransmitter release is secondary to incr sodium entry. /Pyrethroids/ For more Mechanism of Action (Complete) data for CYPERMETHRIN (12 total), please visit the HSDB record page.