Carvacryl acetate
Based on 1 Customer Validation
Carvacryl acetate is an orally active and brain-penetrant TRPA1 receptor activator and Na+/K+-ATPase activator. Carvacryl acetate modulates GABAergic signaling, alters hippocampal GABA and glutamine levels, reduces lipid peroxidation and nitrite formation, scavenges hydroxyl radicals, and boosts glutathione and antioxidant enzyme activity. Carvacryl acetate inhibits Haemonchus contortus larval hatching, development, adult motility, and fecal egg counts, and induces adult worm structural damage. Carvacryl acetate can be used for the research of intestinal mucositis, gastrointestinal nematode infection, epilepsy, and neurodegenerative diseases.
For research use only. We do not sell to patients.
- Purity : 99.83%
- CAS No.: 6380-28-5
- Formula: C12H16O2
- Molecular Weight:192.25
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Storage:Pure form -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
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Biological Activity
Description
IC50 & Target
[1]|
TRPA1 |
In Vitro
Carvacryl acetate binds tightly to the TRPA1 receptor (PDB ID: 3J9P) via stable interactions with eight amino acid residues, with an inhibition constant of 36.8 μM and a binding energy of -6.1 kcal/mol[1].
Carvacryl acetate (0.5-8 mg/mL; 48 h) dose-dependently inhibits Haemonchus contortus egg hatching with an EC50 of 1.7 mg/mL, reaching 89.3% inhibition at 8 mg/mL after 48 h incubation[2].
Carvacryl acetate (0.125-2 mg/mL; 6 days) dose-dependently inhibits Haemonchus contortus larval development with an EC50 of 0.3 mg/mL, reaching 100% inhibition at 2 mg/mL after 6 days of incubation[2].
Carvacryl acetate (25-200 μg/mL; 6 h, 12 h, 24 h) dose- and time-dependently inhibits Haemonchus contortus adult worm motility, achieving 100% inhibition at 200 μg/mL after 24 h of incubation[2].
Carvacryl acetate (200 μg/mL; 24 h) induces structural damage to Haemonchus contortus adult female worms, including cuticle and vulvar flap wrinkling and tegumental bubble formation[2].
Carvacryl acetate (0.9-7.2 μg/mL; 30 min) potently inhibits AAPH-induced lipid peroxidation in egg yolk homogenate, with an EC50 of 0.1785 μg/mL, and shows greater inhibitory activity than Trolox at concentrations ≥1.8 μg/mL[4].
Carvacryl acetate (0.9-7.2 μg/mL; 1 h) scavenges NO generated by SNP in a cell-free system, with an EC50 of 0.1940 μg/mL[4].
Carvacryl acetate (0.9-7.2 μg/mL; 15 min) scavenges Fenton reaction-generated hydroxyl radicals in a cell-free system, with an EC50 of 0.1397 μg/mL, and shows a concentration-dependent inhibitory effect[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
Carvacryl acetate (500-4000 mg/kg; p.o.; single dose) exhibits low acute oral toxicity in female Swiss albino mice, with an LD50 of 1544.5 mg/kg[2].
Carvacryl acetate (250 mg/kg; p.o.; single dose) achieves 65.9% reduction in fecal egg counts in sheep naturally infected with gastrointestinal nematodes at 16 days post single oral 250 mg/kg dose[2].
Carvacryl acetate (100 mg/kg; i.p.; single dose; 30 minutes before Pilocarpine) exerts anticonvulsant effects in Pilocarpine (HY-B0726A)-induced epilepsy in mice, reducing seizures by 60% and mortality by 40%, increasing seizure latency by 340.55%, and improving hippocampal enzyme and GABA levels via a GABAergic-mediated mechanism[3].
Carvacryl acetate (100 mg/kg; i.p.; single dose; 30 minutes before pentylenetetrazol) exerts anticonvulsant effects in pentylenetetrazol-induced epilepsy in mice, reducing seizures and mortality by 70% each, increasing seizure latency by 345.96%, and improving hippocampal enzyme and GABA levels via a GABAergic-mediated mechanism[3].
Carvacryl acetate (100 mg/kg; i.p.; single dose; 30 minutes before Picrotoxin) exerts anticonvulsant effects in Picrotoxin (HY-101391)-induced epilepsy in mice, reducing seizures and mortality by 50% each, increasing seizure latency by 163.67%, and improving hippocampal enzyme and GABA levels via a GABAergic-mediated mechanism[3].
Carvacryl acetate (100 mg/kg; i.p.; single dose) does not alter locomotor activity or motor coordination in healthy mice[3].
Carvacryl acetate (25-100 mg/kg; i.p.; single injection) exhibits potent in vivo antioxidant activity in mouse hippocampus, with the 100 mg/kg dose reducing TBARS levels by 85%, nitrite content by 92%, increasing GSH levels by 50%, and increasing catalase activity by 88% relative to vehicle[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Swiss mice (female, 25-30 g, intestinal mucositis induced via intraperitoneal injection of Irinotecan 75 mg/kg on days 2-5 of an 8-day study)[1]
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Dosage:25 mg/kg; 75 mg/kg; 150 mg/kg
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Administration:i.p.; daily for 8 days
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Result:Achieved 87.5% survival at 25 mg/kg dose.
Achieved 100% survival at 75 mg/kg dose.
Achieved 87.5% survival at 150 mg/kg dose.
Resulted in a body mass loss of 4.6 g over 7 days at 25 mg/kg dose.
Resulted in a body mass loss of 4.4 g over 7 days at 75 mg/kg dose.
Resulted in a body mass loss of 3.4 g over 7 days at 150 mg/kg dose.
Restored leucocyte count to 5710 leucocytes/mm3 at 75 mg/kg dose, reversing CPT-11-induced neutropenia.
Reduced bacterial load to levels comparable to DMSO-treated control mice at 75 mg/kg dose.
Reduced histological injury scores to 0-2 at 75 mg/kg dose, compared to 3-4 in CPT-11-treated mice.
Restored villi height to 185 μm and crypt depth to 86.5 μm at 75 mg/kg dose, reversing CPT-11-induced shortening.
Restored Na+/K+-ATPase activity to 2156 μmol Pi/mg protein/h at 75 mg/kg dose, reversing CPT-11-induced reduction.
Reduced myeloperoxidase (MPO) activity to 1.16 U MPO/mg tissue at 75 mg/kg dose.
Reduced pro-inflammatory cytokine levels to 148.4 pg/mL (IL-1β), 497.9 pg/mL (KC), and 46.24 pg/mL (TNF-α) at 75 mg/kg dose.
Reduced immunostained cells for NF-κB to 23.58 and COX-2 to 12.14 at 75 mg/kg dose.
Reduced malondialdehyde (MDA) to 111.8 nmol/mL and nitric oxide metabolites (NOx) to 0.24 μM at 75 mg/kg dose.
Increased glutathione (GSH) to 610.5 μg/mL and superoxide dismutase (SOD) to 5.04 U SOD/μg at 75 mg/kg dose.
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Animal Model:Swiss albino (female, average weight 25 g)[2]
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Dosage:500 mg/kg; 1000 mg/kg; 2000 mg/kg; 4000 mg/kg
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Administration:p.o.; single dose
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Result:Determined an LD10 of 566.7 mg/kg.
Determined an LD50 of 1544.5 mg/kg.
Showed no behavioral changes in treated mice during the 15-day observation period.
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Animal Model:Sheep (both sexes, 6-16 months old, average weight 18 kg)[2]
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Dosage:250 mg/kg
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Administration:p.o.; single dose
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Result:Reduced fecal egg counts by 35.4% at 8 days post-treatment.
Reduced fecal egg counts by 65.9% at 16 days post-treatment.
Shifted nematode larvae composition from 90% Haemonchus spp., 7% Trichostrongylus spp., 3% Oesophagostumum spp. pre-treatment to 43% Haemonchus spp., 51% Trichostrongylus spp., 6% Oesophagostumum spp. at 16 days post-treatment.
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Animal Model:Swiss albino (male, 25-30 g, 2 months old, Pilocarpine-induced epilepsy)[3]
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Dosage:100 mg/kg
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Administration:i.p.; single dose; 30 minutes before Pilocarpine
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Result:Reduced seizure incidence by 60% and mortality by 40% compared to Pilocarpine-only controls.
Increased latency to first seizure by 340.55% compared to Pilocarpine-only controls.
Increased hippocampal δ-ALA-D activity by 47.35% and Na+, K+-ATPase activity by 30.7% compared to Pilocarpine-only controls.
Increased hippocampal GABA levels by 78.25% compared to Pilocarpine-only controls.
Did not alter glutamate, aspartate, or glutamine levels relative to Pilocarpine-only controls.
Had effects reversed by flumazenil.
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Animal Model:Swiss albino (male, 25-30 g, 2 months old, pentylenetetrazol-induced epilepsy)[3]
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Dosage:100 mg/kg
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Administration:i.p.; single dose; 30 minutes before pentylenetetrazol
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Result:Reduced seizure incidence by 70% and mortality by 70% compared to pentylenetetrazol-only controls.
Increased latency to first seizure by 345.96% compared to pentylenetetrazol-only controls.
Increased hippocampal δ-ALA-D activity by 83.38% and Na+, K+-ATPase activity by 28% compared to pentylenetetrazol-only controls.
Increased hippocampal GABA levels by 51.43% compared to pentylenetetrazol-only controls.
Did not alter glutamate, aspartate, or glutamine levels relative to pentylenetetrazol-only controls.
Had effects reversed by flumazenil.
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Animal Model:Swiss albino (male, 25-30 g, 2 months old, Picrotoxin-induced epilepsy)[3]
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Dosage:100 mg/kg
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Administration:i.p.; single dose; 30 minutes before Picrotoxin
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Result:Reduced seizure incidence by 50% and mortality by 50% compared to Picrotoxin-only controls.
Increased latency to first seizure by 163.67% compared to Picrotoxin-only controls.
Increased hippocampal δ-ALA-D activity by 57.24% and Na+, K+-ATPase activity by 32.6% compared to Picrotoxin-only controls.
Increased hippocampal GABA levels by 103% and reduced glutamine levels by 42.8% compared to Picrotoxin-only controls.
Did not alter glutamate or aspartate levels relative to Picrotoxin-only controls.
Had effects reversed by flumazenil.
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Animal Model:Swiss albino (male, 25-30 g, 2 months old)[3]
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Dosage:100 mg/kg
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Administration:i.p.; single dose
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Result:Produced no significant change in spontaneous locomotor activity compared to vehicle controls.
Produced no significant change in motor coordination compared to vehicle controls.
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Animal Model:Swiss albino (male, 2 months old, 25-30 g)[4]
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Dosage:25 mg/kg; 50 mg/kg; 75 mg/kg; 100 mg/kg
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Administration:i.p.; single injection
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Result:Reduced hippocampal thiobarbituric acid reactive substances (TBARS) levels by 65%, 70%, 72%, and 85% respectively compared to vehicle (p < 0.0001), and by 33%, 43%, 48%, and 71% respectively compared to ascorbic acid 250 mg/kg (p < 0.0001).
Reduced hippocampal nitrite content by 78%, 82%, 85%, and 92% respectively compared to vehicle (p < 0.0001), and by 56%, 65%, 71%, and 85% respectively compared to ascorbic acid 250 mg/kg (p < 0.0001).
Increased hippocampal reduced glutathione (GSH) levels by 26%, 33%, 40%, and 50% respectively compared to vehicle (p < 0.05 for 25, 50, 75 mg/kg; p < 0.001 for 100 mg/kg).
Increased hippocampal glutathione peroxidase (GPx) activity by 49%, 52%, 71%, and 102% respectively compared to vehicle (p < 0.0001); the 75 mg/kg dose was superior to the 50 mg/kg dose (p < 0.001), and the 100 mg/kg dose was superior to the 75 mg/kg dose (p < 0.0001).
Increased hippocampal catalase activity by 57%, 63%, 57%, and 88% respectively compared to vehicle (p < 0.0001).
Did not significantly change hippocampal superoxide dismutase (SOD) activity at any tested dose compared to vehicle.
Chemical Information
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CAS No. 6380-28-5
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Appearance Liquid (Density: 0.994 g/cm3)
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Molecular Weight 192.25
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Formula C12H16O2
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Color Colorless to light yellow
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SMILES
O=C(C)OC1=CC(C(C)C)=CC=C1C
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Pure form -20°C 3 years In solvent -80°C 6 months -20°C 1 month
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (520.16 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: 2.5 mg/mL (13.00 mM); Suspended solution; Need ultrasonic
This protocol yields a suspended solution of 2.5 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.5 mg/mL (13.00 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Purity & Documentation
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Data Sheet (291 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
[1]. Alvarenga EM, et al. Carvacryl acetate, a novel semisynthetic monoterpene ester, binds to the TRPA1 receptor and is effective in attenuating irinotecan-induced intestinal mucositis in mice. J Pharm Pharmacol. 2017;69(12):1773-1785. [Content Brief]
[2]. Andre WP, et al. Comparative efficacy and toxic effects of carvacryl acetate and carvacrol on sheep gastrointestinal nematodes and mice. Vet Parasitol. 2016;218:52-58. [Content Brief]
[3]. Pires LF, et al. Neuropharmacological effects of carvacryl acetate on δ-aminolevulinic dehydratase, Na+, K+-ATPase activities and amino acids levels in mice hippocampus after seizures. Chem Biol Interact. 2015;226:49-57. [Content Brief]
[4]. Pires LF, et al. Is there a correlation between in vitro antioxidant potential and in vivo effect of carvacryl acetate against oxidative stress in mice hippocampus?. Neurochem Res. 2014;39(4):758-769. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
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| DMSO | 1 mM | 5.2016 mL | 26.0078 mL | 52.0156 mL | 130.0390 mL |
| 5 mM | 1.0403 mL | 5.2016 mL | 10.4031 mL | 26.0078 mL | |
| 10 mM | 0.5202 mL | 2.6008 mL | 5.2016 mL | 13.0039 mL | |
| 15 mM | 0.3468 mL | 1.7339 mL | 3.4677 mL | 8.6693 mL | |
| 20 mM | 0.2601 mL | 1.3004 mL | 2.6008 mL | 6.5020 mL | |
| 25 mM | 0.2081 mL | 1.0403 mL | 2.0806 mL | 5.2016 mL | |
| 30 mM | 0.1734 mL | 0.8669 mL | 1.7339 mL | 4.3346 mL | |
| 40 mM | 0.1300 mL | 0.6502 mL | 1.3004 mL | 3.2510 mL | |
| 50 mM | 0.1040 mL | 0.5202 mL | 1.0403 mL | 2.6008 mL | |
| 60 mM | 0.0867 mL | 0.4335 mL | 0.8669 mL | 2.1673 mL | |
| 80 mM | 0.0650 mL | 0.3251 mL | 0.6502 mL | 1.6255 mL | |
| 100 mM | 0.0520 mL | 0.2601 mL | 0.5202 mL | 1.3004 mL |
Carvacryl acetate Related Classifications
HY-N9503 Related Classifications
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