| Size | Price | Stock | Qty |
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| 1mg |
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| 5mg |
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| 10mg |
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| Other Sizes |
| Targets |
The primary molecular target of Moveltipril is angiotensin-converting enzyme (ACE), a key component of the renin-angiotensin system (RAS). ACE is a zinc metallopeptidase responsible for the conversion of the inactive decapeptide angiotensin I to the potent vasoconstrictor octapeptide angiotensin II. By inhibiting ACE, Moveltipril effectively reduces the formation of angiotensin II, leading to vasodilation and a subsequent decrease in blood pressure. This mechanism of action is central to its antihypertensive effects. As a prodrug, Moveltipril itself may have lower intrinsic activity, but its metabolite, captopril, is a well-characterized, potent ACE inhibitor that binds to the active site of the enzyme, blocking its catalytic function.
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| ln Vitro |
The in vitro activity of Moveltipril is primarily defined by its ability to inhibit ACE activity after its conversion to captopril. As a prodrug, Moveltipril is less active in vitro compared to its active metabolite. Studies have shown that Moveltipril is a potent ACE inhibitor, with its efficacy being demonstrated in various biochemical assays that measure the inhibition of ACE-mediated conversion of angiotensin I to angiotensin II. The compound's sulfhydryl group, which is characteristic of captopril and its analogs, is thought to play a crucial role in binding to the zinc ion in the ACE active site, thereby inhibiting the enzyme's activity. The in vitro potency of Moveltipril is consistent with its classification as a newer ACE inhibitor with a favorable pharmacological profile.
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| ln Vivo |
The in vivo activity of Moveltipril is characterized by its antihypertensive effects following oral administration. Due to its partial metabolism to captopril in the liver, Moveltipril provides a sustained reduction in blood pressure compared to captopril. This pharmacokinetic property allows for a slower onset but more prolonged duration of action. In animal models and clinical studies, Moveltipril effectively lowers blood pressure by inhibiting the renin-angiotensin system, leading to decreased peripheral vascular resistance. Its efficacy in managing hypertension has been documented, although its development was eventually discontinued. The compound's activity is a result of its metabolic conversion to the active ACE inhibitor captopril, which then exerts its pharmacological effects systemically.
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| Enzyme Assay |
For in vitro enzyme/receptor binding assays, the activity of Moveltipril is typically assessed by measuring its ability to inhibit ACE. A standard protocol involves using a synthetic substrate, such as hippuryl-histidyl-leucine (HHL), which is cleaved by ACE to produce hippuric acid. The enzyme is incubated with varying concentrations of Moveltipril or its active metabolite, captopril, in a suitable buffer. The reaction is initiated by adding the substrate, and after a specific incubation period, the reaction is stopped, and the amount of hippuric acid produced is measured, often by spectrophotometry or HPLC. The inhibition of ACE activity is calculated by comparing the rate of substrate cleavage in the presence and absence of the inhibitor, allowing for the determination of IC₅₀ values.
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| Cell Assay |
Cell-based in vitro assays for Moveltipril are not typical, as its primary mechanism of action is extracellular, involving the inhibition of the ACE enzyme in the plasma and tissues. However, its activity can be studied in cell culture models that express ACE, such as endothelial cells or other relevant cell lines. In these assays, cells are treated with Moveltipril, and the conversion of exogenous angiotensin I to angiotensin II is measured. The reduction in angiotensin II production, or the subsequent decrease in downstream signaling (e.g., via the angiotensin II type 1 receptor), can be quantified. These experiments help to confirm the compound's mechanism of action and its potency in a more physiologically relevant cellular context.
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| Animal Protocol |
In vivo animal experiments for Moveltipril typically involve the use of rodent models of hypertension, such as spontaneously hypertensive rats (SHR) or angiotensin II-infused models. The compound is administered orally, and its antihypertensive efficacy is assessed by measuring blood pressure at various time points post-administration. The sustained blood pressure reduction observed with Moveltipril is a key endpoint in these studies. Additionally, the effect of the compound on the renin-angiotensin system can be evaluated by measuring plasma renin activity and angiotensin II levels. These studies help to characterize the pharmacokinetic-pharmacodynamic relationship and to confirm the in vivo efficacy of the prodrug.
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| ADME/Pharmacokinetics |
The pharmacokinetic (PK) properties of Moveltipril are distinguished by its partial metabolism in the liver to the active drug captopril. This metabolic conversion contributes to its slower onset but more sustained blood pressure-lowering effect compared to captopril. As an orally active compound, it is absorbed from the gastrointestinal tract. The presence of the sulfhydryl group may also influence its distribution and elimination. The prodrug nature of Moveltipril suggests a more complex PK profile, with the parent compound and its active metabolite both present in the systemic circulation. The sustained action is a result of the gradual release of the active captopril from the prodrug, which may allow for less frequent dosing.
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| Toxicity/Toxicokinetics |
The toxicological profile of Moveltipril is consistent with that of other ACE inhibitors. Common adverse effects associated with this class include hypotension, hyperkalemia, cough, and angioedema. The sulfhydryl group, present in both Moveltipril and captopril, has been associated with a higher incidence of skin rashes and taste disturbances compared to non-sulfhydryl ACE inhibitors. However, specific toxicology data for Moveltipril are limited, as its clinical development was discontinued. Preclinical safety studies would have been conducted to assess its acute and chronic toxicity, genotoxicity, and reproductive toxicity, but these data are not widely published.
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| References | |
| Additional Infomation |
Moveltipril (altiopril calcium, MC-838) is a discontinued ACE inhibitor prodrug that was under development by Chugai Pharmaceutical. It is a structural analog of captopril and is partially metabolized in the liver to captopril. While its development for clinical use was halted, it remains a valuable research tool for studying the renin-angiotensin system and the pharmacology of ACE inhibition. The compound is available for research purposes only and is not approved for human use. Its discontinued status highlights the challenges in drug development, even for compounds with a well-understood mechanism of action. No clinical trials or regulatory approvals exist for Moveltipril.
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| Molecular Formula |
2[C19H29N2O5S-].CA+2
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| Molecular Weight |
835.095920000001
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| Exact Mass |
398.188
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| CAS # |
85856-54-8
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| Related CAS # |
85921-53-5 (calcium salt);
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| PubChem CID |
6321426
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| Appearance |
White to off-white solid powder
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| Density |
1.248g/cm3
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| Boiling Point |
658.9ºC at 760 mmHg
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| Melting Point |
113-116°
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| Flash Point |
352.3ºC
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| Index of Refraction |
1.553
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| LogP |
2.371
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
6
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| Rotatable Bond Count |
8
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| Heavy Atom Count |
27
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| Complexity |
576
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| Defined Atom Stereocenter Count |
3
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| SMILES |
C[C@H](CSC(=O)[C@@H](C)NC(=O)C1CCCCC1)C(=O)N2CCC[C@H]2C(=O)O
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| InChi Key |
QIJLJZOGPPQCOG-NFAWXSAZSA-N
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| InChi Code |
InChI=1S/C19H30N2O5S/c1-12(17(23)21-10-6-9-15(21)18(24)25)11-27-19(26)13(2)20-16(22)14-7-4-3-5-8-14/h12-15H,3-11H2,1-2H3,(H,20,22)(H,24,25)/t12-,13-,15+/m1/s1
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| Chemical Name |
(2S)-1-[(2S)-3-[(2R)-2-(cyclohexanecarbonylamino)propanoyl]sulfanyl-2-methylpropanoyl]pyrrolidine-2-carboxylic acid
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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 : ~100 mg/mL (~250.93 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (6.27 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 25.0 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: ≥ 2.5 mg/mL (6.27 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 25.0 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: ≥ 2.5 mg/mL (6.27 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 | 1.1975 mL | 5.9873 mL | 11.9746 mL | |
| 5 mM | 0.2395 mL | 1.1975 mL | 2.3949 mL | |
| 10 mM | 0.1197 mL | 0.5987 mL | 1.1975 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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