Carvacryl acetate
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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.
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- 純度 : 99.83%
- CAS 番号: 6380-28-5
- 分子式: C12H16O2
- 分子量:192.25
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保管条件:Pure form -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
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生物活性
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生物活性
製品説明
IC50 & Target
[1]|
TRPA1 |
体外実験
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. Further protocols information, click here.
体内実験
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.
化学情報
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CAS 番号 6380-28-5
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性状 Liquid (Density: 0.994 g/cm3)
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分子量 192.25
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分子式 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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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Pure form -20°C 3 years In solvent -80°C 6 months -20°C 1 month
プロトコル
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
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Ferroptosis Solutions
Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death characterized by lethal lipid peroxidation and sensitivity to suppression by iron chelators or lipophilic radical-trapping antioxidants. The core pathway links cystine uptake through system Xc−, glutathione availability, GPX4-dependent detoxification of phospholipid hydroperoxides, iron-dependent oxidative reactions, and polyunsaturated-phospholipid metabolism into a cell-death program that is biochemically and morphologically distinct from apoptosis, necrosis, and autophagy. The ferroptosis pathway is experimentally linked to phenotype through chemical and genetic perturbation. Erastin induces ferroptosis by inhibiting cystine uptake through system Xc− and weakening antioxidant defenses, while GPX4 inhibition or depletion causes lipid peroxide accumulation and ferroptotic cancer-cell death. ACSL4 and oxidizable arachidonoyl- or adrenoyl-containing phosphatidylethanolamines shape ferroptosis sensitivity by con
純度とドキュメンテーション
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取扱説明書 (2659 KB)
参考文献
[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]
Calculators
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Carvacryl acetate 関連分類
HY-N9503 関連分類
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