| Size | Price | Stock | Qty |
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| 100mg |
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| 250mg |
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| 500mg |
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| Other Sizes |
| Targets |
The primary target of Cinromide is the epithelial neutral amino acid transporter B0AT1 (SLC6A19). Cinromide inhibits B0AT1 with an IC50 of 0.5 µM. B0AT1 is a transporter responsible for the absorption of neutral amino acids in the intestine and kidney. By inhibiting B0AT1, Cinromide may modulate amino acid levels and affect neurotransmitter balance, which could contribute to its anticonvulsant effects. The compound's mechanism of action as a B0AT1 inhibitor is distinct from other anticonvulsants, making it a valuable tool for studying amino acid transport and epilepsy.
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| ln Vitro |
In rats, 5-HT-induced fundus strip contraction is 46% inhibited by cinromide (10-100 μM). Monoamine oxidase produced from rat liver and brain is inhibited by cinromide (100 μM) [3].
Cinromide is an inhibitor of the epithelial neutral amino acid transporter B0AT1 with an IC50 of 0.5 µM. As an anticonvulsant drug, it exhibits protection of the nervous system. The compound's inhibition of B0AT1 may modulate amino acid levels and affect neurotransmitter balance, which could contribute to its anticonvulsant effects. Its activity as a B0AT1 inhibitor makes it a valuable tool for studying amino acid transport and related physiological processes. |
| ln Vivo |
In mice, cinromide causes electroconvulsions and pentetrazo1-induced convulsions, with ED50 values of 60±11 mg/kg, 90±15 mg/kg, and 80±15 mg/kg, 300± 61 mg/kg, correspondingly. After being administered intraperitoneally to rats, cinromide exhibited dose-related action against tepstatazol, with an ED50 of 58 ± 11 mg/kg. Moreover, in an intravenous leptamazole threshold test in rats, cinromide (75 mg/kg) markedly raised the leptamazole concentration needed to cause clonic seizures. Cinromide (300 mg/kg, i.p.) did not significantly affect dogs who were sedated and left with their chests open four hours after treatment, nor did it significantly affect dogs that were awake five hours after oral dose of 300 and 600 mg/kg. cinromide [1]. Neuronal responses to unconditioned maxillary nerve stimulation are inhibited by cinromide (40 mg/kg, IV), which increases latency and decreases spike counts. Segmental inhibition and the latency of unconditioned responses are both dose-dependently increased by cinromide (20, 40, 80 mg/kg, iv). Electroencephalogram and periventricular inhibition are reduced by sinromid [4].
Cinromide is an anticonvulsant drug that exhibits protection of the nervous system. By inhibiting B0AT1, it may modulate amino acid levels and affect neurotransmitter balance, which could contribute to its anticonvulsant effects in vivo. The compound's potential applications in treating epilepsy and other neurological disorders would require evaluation in appropriate in vivo models. However, specific in vivo studies have not been detailed in the available literature. |
| Enzyme Assay |
No specific non-cell assay protocol is available for Cinromide. For transporter inhibitors, standard cell-free assays include radioligand binding or transport assays using membrane preparations from cells expressing recombinant B0AT1. The compound's inhibition of radiolabeled amino acid uptake or binding can be measured to determine IC50 values. These assays provide quantitative data on the compound's affinity for B0AT1.
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| Cell Assay |
No specific cell-based assay protocol is available for Cinromide. For transporter inhibitors, standard cellular assays use cells expressing recombinant B0AT1. Cells are treated with Cinromide in the presence of radiolabeled or fluorescent amino acids, and amino acid uptake is measured. The compound's inhibition of amino acid uptake is measured to determine IC50 values. Selectivity for B0AT1 over other amino acid transporters can be assessed using cells expressing related transporters.
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| Animal Protocol |
No specific animal protocol is available for Cinromide. For anticonvulsant studies, standard in vivo models include chemically induced seizures (e.g., pentylenetetrazole, maximal electroshock) or genetically epilepsy-prone models. Cinromide is administered (route and dose to be determined) prior to seizure induction. Seizure parameters (latency, duration, severity) and survival are recorded. The compound's effects on amino acid levels in the brain and other tissues can also be assessed.
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| ADME/Pharmacokinetics |
No detailed pharmacokinetic data is publicly available for Cinromide. The compound has a molecular weight of 254.12 and formula C11H12BrNO. As a small molecule with moderate lipophilicity, it would be expected to have reasonable oral bioavailability and blood-brain barrier penetration. The compound is a cinnamamide derivative with potential for CNS activity. Comprehensive pharmacokinetic studies would be required for therapeutic development.
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| Toxicity/Toxicokinetics |
No detailed toxicology data is publicly available for Cinromide. As an anticonvulsant drug candidate, standard preclinical toxicology would be required for therapeutic development. The compound's mechanism of action as a B0AT1 inhibitor suggests potential effects on amino acid homeostasis that would need to be carefully evaluated. The compound is for research use only and not for therapeutic applications.
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| References |
[1]. Chiu P, et al. The effect of cinromide on "kindled" seizures in the rat. Neuropharmacology. 1982;21(3):273-276.
[2]. Yadav A, et al. Novel Chemical Scaffolds to Inhibit the Neutral Amino Acid Transporter B0AT1 (SLC6A19), a Potential Target to Treat Metabolic Diseases. Front Pharmacol. 2020;11:140. Published 2020 Feb 28. [3]. Soroko FE, et al. Cinromide (3-bromo-N-ethylcinnanamide), novel anticonvulsant agent. J Pharm Pharmacol. 1981 Nov;33(11):741-3. [4]. Fromm GH, et al. Effect of cinromide on inhibitory and excitatory mechanisms. Epilepsia. 1983 Aug;24(4):394-400 |
| Additional Infomation |
Cinnamamide belongs to the cinnamamide class of compounds and is a secondary carboxylamide.
Cinromide is also known as trans-3-bromo-N-ethylcinnamamide and (2E)-3-(3-Bromophenyl)-N-ethyl-2-propenamide. It has the molecular formula C11H12BrNO and molecular weight 254.12. The IUPAC name is (E)-3-(3-bromophenyl)-N-ethylprop-2-enamide. It is an anticonvulsant drug and an inhibitor of the epithelial neutral amino acid transporter B0AT1 (SLC6A19) with an IC50 of 0.5 µM. No clinical trial status has been identified; it is used for research purposes. |
| Molecular Formula |
C11H12BRNO
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| Molecular Weight |
254.127
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| Exact Mass |
253.01
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| CAS # |
58473-74-8
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| PubChem CID |
688145
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| Appearance |
Typically exists as solid at room temperature
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| Density |
1.369g/cm3
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| Boiling Point |
417.5ºC at 760mmHg
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| Melting Point |
89-91ºC(lit.)
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| Flash Point |
206.3ºC
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| Index of Refraction |
1.591
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| LogP |
2.989
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
1
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| Rotatable Bond Count |
3
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| Heavy Atom Count |
14
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| Complexity |
215
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| Defined Atom Stereocenter Count |
0
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| SMILES |
BrC1=C([H])C([H])=C([H])C(=C1[H])/C(/[H])=C(\[H])/C(N([H])C([H])([H])C([H])([H])[H])=O
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| InChi Key |
LDCXGZCEMNMWIL-VOTSOKGWSA-N
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| InChi Code |
InChI=1S/C11H12BrNO/c1-2-13-11(14)7-6-9-4-3-5-10(12)8-9/h3-8H,2H2,1H3,(H,13,14)/b7-6+
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| Chemical Name |
(E)-3-(3-bromophenyl)-N-ethylprop-2-enamide
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| Synonyms |
Vumide; Cinromide
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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) |
DMSO : ~250 mg/mL (~983.79 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (8.19 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.08 mg/mL (8.19 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.08 mg/mL (8.19 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.9350 mL | 19.6750 mL | 39.3499 mL | |
| 5 mM | 0.7870 mL | 3.9350 mL | 7.8700 mL | |
| 10 mM | 0.3935 mL | 1.9675 mL | 3.9350 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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