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| Targets |
D-Phenothrin exerts its insecticidal effect by targeting the voltage-gated sodium channels in the neuronal membranes of insects. The compound binds to the alpha-subunit of these channels, specifically prolonging the opening of the channels and preventing their normal inactivation. This binding locks the channel in an open state, leading to a continuous influx of sodium ions into the nerve cell. The resulting prolonged depolarization causes hyper-excitation of the nervous system, which manifests as repetitive nerve firing, tremors, paralysis, and ultimately death of the insect. This mechanism is characteristic of Type I pyrethroids, which are distinguished from Type II pyrethroids by the absence of a cyano group and a different symptomology. The compound's high insecticidal potency is attributed to its high affinity for the insect sodium channel, which is structurally different from the mammalian sodium channel, contributing to its selective toxicity. D-Phenothrin's action is fast-acting, and it is effective against a wide range of insect pests due to the conserved nature of sodium channels across insect species.
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| ln Vitro |
The in vitro activity of D-Phenothrin is primarily assessed through receptor binding assays using insect neural membrane preparations. Radiolabeled ligands, such as [³H]saxitoxin or [³H]batrachotoxin, which bind to the sodium channel, are used to assess the compound's binding affinity. D-Phenothrin competes with these ligands for binding sites on the sodium channel, and its IC₅₀ is determined by measuring the displacement of the radiolabeled ligand. The compound exhibits high affinity for the insect sodium channel, which correlates with its potent insecticidal activity. In cell-based assays using insect cell lines such as Sf9 or Drosophila Schneider 2 cells, D-Phenothrin demonstrates cytotoxicity with an EC₅₀ typically in the micromolar range. The compound's activity is time- and concentration-dependent, with longer exposure times and higher concentrations leading to increased cell death. The in vitro activity is often used as a predictor of in vivo efficacy. The compound's insecticidal activity is also evaluated in topical application assays on insects, where the LD₅₀ (lethal dose for 50% of the population) is determined.
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| ln Vivo |
The intraperitoneal injection of D-phemethrin ((-)-trans-phenothrin; 25-200 mg/kg; administered for 14 days) markedly and dose-dependently enhanced oxidative DNA damage in both animal organs [1]. D-phemethrin does not have any negative estrogenic or (anti)androgenic effects when taken orally for three days at doses of 100, 300, or 1000 mg/kg [2].
D-Phenothrin exhibits potent in vivo insecticidal activity against a wide range of pests. In field studies and controlled laboratory experiments, the compound demonstrates high efficacy in controlling mosquito populations, particularly Anopheles species, which are vectors of malaria. Ultra-low volume (ULV) applications of D-Phenothrin combined with residual spraying have been shown to significantly reduce Anopheles albimanus populations. The compound is also effective against houseflies, cockroaches, fleas, ticks, and head lice. Its in vivo efficacy is attributed to its rapid action and broad-spectrum activity. The compound's oral bioavailability allows for its use in oral formulations for veterinary applications. In agricultural settings, D-Phenothrin is used to protect crops from damage by various pests, and it is often integrated into pest management strategies to minimize the development of resistance. The compound's efficacy is influenced by factors such as formulation, application method, and environmental conditions. Despite its potent insecticidal activity, D-Phenothrin has a relatively poor knockdown effect, which may delay the visible paralysis of insects. |
| Enzyme Assay |
In vitro receptor binding assays are used to study the interaction of D-Phenothrin with its target, the voltage-gated sodium channel. Membrane preparations are typically obtained from insect neural tissues, such as housefly heads or cockroach nerve cords. The membranes are incubated with a radiolabeled ligand, such as [³H]saxitoxin or [³H]batrachotoxin, which binds to a specific site on the sodium channel. Varying concentrations of D-Phenothrin are added to the reaction mixture to compete with the radiolabeled ligand for binding. After incubation, the membranes are collected by filtration, and the bound radioactivity is measured using a scintillation counter. The amount of radiolabeled ligand bound is inversely proportional to the concentration of D-Phenothrin. The IC₅₀, which is the concentration of D-Phenothrin required to displace 50% of the radiolabeled ligand, is determined from the competition curve. This assay provides a direct measure of the compound's affinity for the sodium channel. To assess selectivity, similar assays can be performed using mammalian brain membranes. The difference in affinity between insect and mammalian sodium channels is a key factor in the selective toxicity of pyrethroids.
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| Cell Assay |
For in vitro cell-based assays, insect cell lines such as Sf9 (from Spodoptera frugiperda) or Drosophila Schneider 2 cells are commonly used. Cells are seeded in 96-well plates at a density of approximately 1-2 × 10⁴ cells per well and allowed to attach overnight. The cells are then exposed to serial dilutions of D-Phenothrin in culture medium for a period of 24-48 hours. Cytotoxicity is assessed using a colorimetric assay such as MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) or a luminescent assay such as ATP-lite. In the MTT assay, viable cells with active mitochondria reduce MTT to a purple formazan product, which is solubilized and measured spectrophotometrically. The absorbance is directly proportional to the number of viable cells. The percentage of cell viability at each compound concentration is calculated relative to untreated control cells. The EC₅₀, representing the concentration that reduces cell viability by 50%, is determined from the dose-response curve. These assays provide a measure of the compound's cytotoxic potential and are used to evaluate its activity against insect cells.
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| Animal Protocol |
Animal/Disease Models: Male Wistar albino rat (6 weeks old, 150-200 g)
Doses: 25, 50, 100, 200 mg/kg Route of Administration: IP; 14 days Experimental Results: Oxidative DNA damage appeared in two organs of the animal Statistically significant and dose-dependent increase. In vivo insecticidal efficacy is assessed through topical application or spray tests on target insects such as houseflies (Musca domestica) or mosquitoes (Aedes aegypti or Anopheles species). In a typical topical application assay, a small volume (1-2 μL) of a solution containing D-Phenothrin at various concentrations in a suitable solvent (e.g., acetone) is applied to the dorsal thorax of the insect using a micro-applicator. A control group receives the solvent alone. The insects are then held in a controlled environment, and mortality is recorded at 24 and 48 hours post-treatment. The LD₅₀, which is the dose required to kill 50% of the insect population, is calculated using probit analysis. In spray tests, the compound is formulated as an aqueous spray and applied to insects or surfaces. The efficacy is evaluated by measuring the percentage of insects killed or knocked down. For mosquito control, field studies involve ULV applications of the compound in affected areas, and the reduction in mosquito populations is monitored using traps and other surveillance methods. These in vivo assays provide critical data on the compound's practical efficacy and are essential for its registration and use as an insecticide. |
| ADME/Pharmacokinetics |
D-Phenothrin, as a synthetic pyrethroid, is highly lipophilic and is rapidly metabolized in mammals via ester hydrolysis and oxidation. The compound is orally bioavailable, allowing for its use in oral formulations for veterinary applications. Due to its rapid metabolic clearance in mammals, the compound has low oral toxicity. The primary route of metabolism involves cleavage of the ester bond by carboxylesterases, yielding inactive metabolites that are readily excreted. The compound's logP value, which is relatively high, indicates good tissue penetration and distribution. However, specific pharmacokinetic parameters such as half-life (t₁/₂), volume of distribution (Vd), and clearance (CL) are not extensively detailed in the available literature. The compound's rapid metabolism and elimination in mammals contribute to its favorable safety profile, as it does not accumulate in the body. In insects, the compound's metabolism is slower, which contributes to its insecticidal potency. The compound's stability to light is an important factor for its use in outdoor applications, as it allows for longer residual activity.
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| Toxicity/Toxicokinetics |
D-Phenothrin exhibits low acute toxicity in mammals. The oral LD₅₀ in rats is reported to be in the range of 25-200 mg/kg, indicating that it is one of the least toxic pyrethroids. It is considered safe for use in public health and veterinary applications when used according to label instructions. The compound is not a skin sensitizer and is not classified as a carcinogen. However, as with all pyrethroids, it can cause skin and eye irritation upon direct contact. In case of ingestion, symptoms may include nausea, vomiting, and neurological effects such as tremors, but these are generally reversible. The compound is toxic to fish and aquatic invertebrates, and it should be used with caution near water bodies. It is also toxic to bees, and applications should be timed to minimize exposure to these beneficial insects. Despite its low mammalian toxicity, long-term exposure to chemical pesticides has been associated with potential health issues, including neurological disorders, and safety guidelines should be followed during application. D-Phenothrin is approved by the WHO for use as a public health insecticide and is the only pyrethroid permitted for use on US commercial aircraft. It is not approved for human therapeutic use.
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| References |
[1]. Atmaca E, et al. d-Phenothrin-induced oxidative DNA damage in rat liver and kidney determined by HPLC-ECD/DAD. Environ Toxicol. 2015 May;30(5):607-13.
[2]. Yamada T, et al. Lack of estrogenic or (anti-)androgenic effects of d-phenothrin in the uterotrophic and Hershberger assays. Toxicology. 2003 Apr 22;186(3):227-39. |
| Additional Infomation |
(1R)-trans-pyrethrin is a pyrethrin. It is functionally related to (+)-trans-chrysanthemic acid.
See also: Pyrethrin (note moved to). |
| Molecular Formula |
C₂₃H₂₆O₃
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|---|---|
| Molecular Weight |
350.45
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| Exact Mass |
350.188
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| CAS # |
26046-85-5
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| Related CAS # |
Phenothrin;26002-80-2
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| PubChem CID |
91581
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| Appearance |
Typically exists as solid at room temperature
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| Density |
1.12 g/cm3
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| Boiling Point |
437ºC at 760 mmHg
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| Flash Point |
186.6ºC
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| Vapour Pressure |
0mmHg at 25°C
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| Index of Refraction |
1.588
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| LogP |
5.76
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| Hydrogen Bond Donor Count |
0
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| Hydrogen Bond Acceptor Count |
3
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| Rotatable Bond Count |
7
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| Heavy Atom Count |
26
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| Complexity |
512
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| Defined Atom Stereocenter Count |
2
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| SMILES |
CC(=C[C@@H]1[C@@H](C(=O)OCC2=CC(=CC=C2)OC3=CC=CC=C3)C1(C)C)C
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| InChi Key |
SBNFWQZLDJGRLK-RTWAWAEBSA-N
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| InChi Code |
InChI=1S/C23H26O3/c1-16(2)13-20-21(23(20,3)4)22(24)25-15-17-9-8-12-19(14-17)26-18-10-6-5-7-11-18/h5-14,20-21H,15H2,1-4H3/t20-,21+/m1/s1
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| Chemical Name |
(3-phenoxyphenyl)methyl (1R,3R)-2,2-dimethyl-3-(2-methylprop-1-enyl)cyclopropane-1-carboxylate
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| Synonyms |
DPhenothrin; D Phenothrin
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.8535 mL | 14.2674 mL | 28.5347 mL | |
| 5 mM | 0.5707 mL | 2.8535 mL | 5.7069 mL | |
| 10 mM | 0.2853 mL | 1.4267 mL | 2.8535 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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