PARA SPECIAL LICE SPRAY

Indications

• Lice infestation (pediculosis)
• Scabies
• Other ectoparasitic infestations

Dosage

Children: Refer to specific product labeling for paediatric dosing instructions.

Adults: Refer to specific product labeling for adult dosing instructions.

Mechanism of action

Bioallethrin, like other pyrethroids, binds to voltage-gated sodium channels in their closed state, modifying the gating kinetics. This binding increases the channel's affinity for pyrethroids, resulting in prolonged opening and delayed closing of the sodium channel. These changes heighten the neuron's susceptibility to action potentials, causing repeated firing, which ultimately leads to the release of excessive neurotransmitters. In ectoparasites, this results in respiratory paralysis and death. Additionally, bioallethrin can block certain types of calcium channels, contributing to its insecticidal effects.

Pharmacodynamics

Bioallethrin causes respiratory paralysis in lice and scabies parasites, leading to their death. The drug's action on sodium and calcium channels disrupts the normal excitability of neuronal membranes, facilitating the insect's inability to function properly and ultimately resulting in paralysis.

Pharmacokinetics

The pharmacokinetics of bioallethrin are characterized by its rapid absorption and distribution in biological systems. It is metabolized primarily in the liver and excreted through urine and feces. Due to its lipophilic nature, bioallethrin has a tendency to accumulate in fatty tissues, although it is generally eliminated efficiently from the body.

Pregnancy

Bioallethrin should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Consult a healthcare professional for advice.

Breast-feeding

Use of bioallethrin while breastfeeding should be approached with caution. Consult a healthcare professional before use.

Storage

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

Formulations

• Topical solutions
• Aerosol sprays

Indications

• Synergist in pesticide formulations
• Enhancement of insecticidal activity

Dosage

Children: Refer to specific pesticide formulations for guidance, as piperonyl butoxide is not used as a standalone medication.

Adults: Refer to specific pesticide formulations for guidance, as piperonyl butoxide is not used as a standalone medication.

Mechanism of action

Piperonyl butoxide acts as a synergist by inhibiting the mixed-function oxidase (MFO) system of insects, which enhances the activity of pesticides and allows for lower doses of insecticides to be used effectively. This mechanism increases the levels of insecticides within the target organism, thereby improving their lethality without increasing the dosage of the insecticide.

Pharmacodynamics

Piperonyl butoxide does not affect the mixed-function oxidase system in humans and has shown no significant effects in small trials involving human volunteers. Its primary action is limited to insects, where it enhances the toxicity of certain insecticides by preventing their breakdown.

Pharmacokinetics

The pharmacokinetics of piperonyl butoxide in humans is not well-studied, and it does not significantly interact with human metabolic pathways like the mixed-function oxidase system. Its effects are predominantly observed in insects where it alters the metabolism of co-administered pesticides.

Pregnancy

Piperonyl butoxide should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Data on the effects of piperonyl butoxide in pregnant women are limited.

Breast-feeding

There is insufficient data on the excretion of piperonyl butoxide in human milk. Caution should be exercised when administering to breastfeeding women.

Storage

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

Formulations

• Piperonyl butoxide 30% concentration for agricultural use
• Piperonyl butoxide formulations combined with insecticides such as pyrethrins and carbamates

Indications

• Schizophrenia
• Agitation
• Sleep disorders

Dosage

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

Adults: Refer to the BNF for specific dosing guidelines.

Mechanism of action

Pipamperone binds mainly to 5-HT2A receptors, with significant affinity for D4 receptors and moderate affinity for 5-HT2C, D2, D3, and 1- and 2B-adrenoceptors. As a selective 5-HT2A, D1, and D4 antagonist, it demonstrates a 15-fold higher affinity for D4 than D2 receptors. This selectivity is believed to limit extrapyramidal side effects and modulate GABAergic neuronal activity.

Pharmacodynamics

Pipamperone is characterized by its antipsychotic, sedative, and anti-agitation effects. By exhibiting antidopaminergic and anti-serotonergic properties, it is effective in normalizing sleep patterns and reducing positive psychotic symptoms, including delusions and hallucinations. Increased expression of D4 receptors has been associated with its therapeutic effects.

Pharmacokinetics

The pharmacokinetics of pipamperone include absorption, distribution, metabolism, and excretion characteristics typical of atypical antipsychotics, although specific parameters such as half-life and clearance rates are not provided in the sources. It is important for clinicians to monitor the drug's therapeutic levels and adjust dosages accordingly to achieve optimal treatment outcomes.

Adverse effects

• Sedation
• Dizziness
• Extrapyramidal symptoms
• Weight gain
• Dry mouth
• Hypotension

Precautions

• Caution in patients with a history of seizures
• Monitor for signs of tardive dyskinesia
• Use cautiously in elderly patients

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 pipamperone is excreted in human milk. Caution is advised when administering to nursing mothers.

Storage

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

Formulations

• Tablets
• Oral solution

Mechanism of action

Bioallethrin, like other pyrethroids, binds to voltage gated sodium channels in their closed state and modifies the gating kinetics. Channel opening appears to increase affinity of the channel for pyrethroids like bioallethrin. Once bound pyrethroids slow both the opening and closing of the sodium channel resulting in a need for stronger excitatory potentials to produce an action potential and a delay in repolarization. The these changes make the neuron more susceptible to large action potentials and repeated firing by both increasing the initial threshold and reducing the input needed for after-potentials. When repeated firing does occur, the nerve terminal will release more neurotransmitter which can produce muscle paralysis through tetanus. This paralysis stops the breathing of lice and scabies parasites resulting in death. Some pyrethroids act on calcium channels to increase intracelllular calcium. Bioallethrin produces a very small increase in intracellular calcium in mouse neocortical neurons by acting on N-type calcium channels but the effect returns to baseline within 2 min. In contrast bioallethrin has been found to block L T, and P/Q-types of voltage gated calcium channels in human embryonic kidney cell cultures. Bioallethrin has been found to inhibit both sodium-calcium dependent and magnesium-calcium ATP hydrolysis in insects although it, along with other type I pyrethroids, has a greater effect on sodium-calcium dependent hydrolysis. Bioallethrin may stimulate phosphoinositol breakdown in synaptoneuromes as other type I pyrethroids have been observed to do so. Other type I pyrethoids have also been found to bind to kainate receptors.

Pharmacodynamics

Bioallethrin causes respiratory paralysis in lice and scabies parasites resulting in death.

Mechanism of action

Piperonyl butoxide is not a pesticide, but acts as a synergist to increase the activity of pesticides such as carbamates, pyrethrins, pyrethroids, and rotenone. Piperonyl butoxide inhibits the mixed-function oxidase (MFO) system of an insect. The MFO system is the insects natural defense system and causes the oxidative breakdown of insecticides. Thus, by inhibiting this system piperonyl butoxide promotes higher levels of insecticide and allows for lower doses to be used for a lethal effect. To clarify the mechanism of piperonyl butoxide (PBO)-induced hepatocarcinogenesis in mice, male mice were subjected to a two-thirds partial hepatectomy, N-diethylnitrosamine (DEN) initiation, and a diet containing 0.6% PBO for eight weeks. The incidence of gamma-glutamyl transpeptidase (GGT)-positive foci and PCNA-positive cells was significantly increased in the DEN + PBO group compared with the DEN-alone group. Real-time reverse transcription-polymerase chain reaction (RT-PCR) analysis showed up-regulation of genes related to metabolism, such as cytochrome P450 1A1 and 2B10, and metabolic stress, such as Por, Nqo1, Nrf2, abcc3, and abcc4. Early responsive genes downstream of mitogen-activated protein kinase (MAPK), such as c-fos, c-jun, c-myc, and activating transcription factor 3 (ATF3), were also up-regulated in this group. Positive immunohistochemical staining for ATF3 was diffusely observed in nonproliferating hepatocytes of the DEN + PBO group, but altered foci were negative or weakly positive for ATF3. The nuclei of hepatocytes within ATF3-negative foci were positive for cyclin D. Thus PBO can induce oxidative stress, activate the MAPK pathway, and increase ATF3 transcript levels in hepatocytes outside the altered foci during the early stage of PBO-induced hepatocarcinogenesis in mice. . ... Male F344 rats were administered piperonyl butoxide mixed in the diet at concentrations of 0 (negative control), 0.05, 0.2 or 2% for 2 days, 1, 2, and 4 weeks. As a positive control, phenobarbital was administered to rats for up to 4 weeks as a 0.1% solution in the drinking water. Increased liver weight, centrilobular hepatocellular hypertrophy due to increased smooth endoplasmic reticulum, decreased numbers and areas of connexin 32-positive spots per hepatocyte, and increased cell proliferation were observed in rats treated with 0.2 and 2% piperonyl butoxide. Similar results were obtained for 0.1% phenobarbital treated rats. Hepatocellular necrosis suggestive of hepatotoxicity was also observed in the 2% piperonyl butoxide group. These results indicate that the promoting mechanism of piperonyl butoxide in hepatocarcinogenesis is similar to that of phenobarbital, involving an ability to induce CYP isoenzymes and inhibit gap junctional intercellular communication. In addition, increased cell proliferation following hepatocellular necrosis may also play a role at high doses. Piperonyl butoxide (PBO) is an insecticide synergist known to inhibit the activity of cytochrome P450 enzymes. ... Little is known about how insects respond to PBO exposure at the gene transcription level. The authors have characterized the transcriptional response of the Drosophila melanogaster genome after PBO treatment, using both a custom-designed 'detox' microarray, containing cytochrome P450 (P450), glutathione S-transferase (GST) and esterase genes, and a full genome microarray. A subset of P450 and GST genes is identified, along with additional metabolic genes, that are induced by PBO. The gene set is an extremely similar gene set to that induced by phenobarbital, a compound for which pretreatment is known to confer tolerance to a range of insecticide compounds. Piperonyl butoxide (PBO), alpha-[2-(2-butoxyethoxy)ethoxy]-4,5-methylene-dioxy-2-propyltoluene, is widely used as a synergist for pyrethrins. In order to clarify the possible mechanism of non-genotoxic hepatocarcinogenesis induced by PBO, molecular pathological analyses consisting of low-density microarray anal

Pharmacodynamics

Piperonyl butoxide does not affect the mixed-function oxidase system in humans. In small trials in human volunteers, usual doses of piperonyl butoxide had no effect on humans.

Mechanism of action

Pipamperone binds mainly to 5-HT2A receptors, with a nearly equal affinity to D4 receptors and a moderate affinity for 5-HT2C, D2, D3, 1- and 2B-adrenoceptors. This drug is a selective 5-HT2A, D1 and D4 antagonist. Extrapyramidal adverse effects also appear to be limited in pipamperone treatment compared to traditional antipsychotic medications due to its high receptor selectivity. Pipamperone has a 15-fold higher affinity for D4 than D2 receptors. It has been suggested that D4 receptors may play a role in the modulation of GABAergic neuronal activity by dopamine.

Pharmacodynamics

Pipamperone is an antipsychotic medication that has sedative effects, which may be beneficial in the management of agitation and disordered sleep. Pipamperone, showing antidopaminergic and anti-serotonergic properties, has been noted for its anti- agitation effects and for its ability to normalize sleep rhythms in psychiatric patients. One study showed that pipamperone increased the expression of D4 (dopaminergic) receptors, explaining its helpfulness in decreasing positive psychotic symptoms, such as delusions and hallucinations.