Moexipril has little effect on platelet function and no anti-inflammatory qualities [2]. When moexipril is hydrolyzed, moexiprilat is produced, which inhibits ACE in rabbit lung and guinea pig serum with IC50 values of 2.6 nM and 4.9 nM, respectively [2]. With IC50 values of 1.75 nM and 2.1 nM, respectively, moexipril (0.01 nM-0.1 mM) demonstrated strong efficacy against ACE in rat plasma and pure ACE in rabbit lung [3]. In a dose-dependent manner, moexipril (0-100 μM) considerably lowers the percentage of injured neurons in 24 hours [4]. Neurotoxicity produced by Fe2+/3+ can be considerably reduced by moexipril (0-100 μM, 24 hours) [4]. The fraction of apoptotic neurons is not significantly affected by moexipril dosage [4].

The blood-brain barrier is impervious to moexipril [1]. Moexipril had antihypertensive and dose-dependent effects when taken orally once daily for five days at dosages of 3 mg/kg, 30 mg/kg, and 10 mg/kg[3]. The infarct area on the brain surface of NMRI mice is dramatically reduced by moexipril (0.3 mg/kg, intraperitoneal injection) [4]. In Long-Evans rats, intraperitoneal injections of moexipril (0.1 mg/kg) can significantly reduce the volume of cortical infarcts [4].

Animal/Disease Models: Spontaneously hypertensive rats [3]
Doses: 30 mg/kg
Route of Administration: po (oral gavage); one time/day; 5 days
Experimental Results: The average blood pressure gradually diminished from 180 +/- 7 mmHg before treatment to the third 4 days of lows of 127 +/- 4 mmHg. Dose-dependently reduces arterial blood pressure and inhibits plasma and tissue ACE activity.

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Animal/Disease Models: Renal hypertension rats [3]
Doses: 0.03-10 mg/kg
Route of Administration: po (oral gavage); one time/day; 5 days
Experimental Results: Caused a dose-dependent decrease in blood pressure, with a threshold dose of 0.3 mg/kg . The average blood pressure decreases by 3 mg/kg to approximately 70 mmHg.

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Animal/Disease Models: Perinephritis hypertensive dogs [3]
Doses: 10 mg/kg
Route of Administration: po (oral gavage); one time/day; 5 days
Experimental Results: Due to the rapid onset of action and long duration of action, the average blood pressure dropped by 25 mmHg compared with the control before treatment , lasts 24 hrs (hrs (hours)).

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Animal/Disease Models: NMRI mouse (male, permanent focal ische

Absorption, Distribution and Excretion
Moexipril is not completely absorbed; the bioavailability of its metabolite, Moexiprilat, is approximately 13% of that of intravenously administered Moexipril (both measured by the metabolite Moexiprilat), and is significantly affected by food intake. After consuming a low-fat breakfast, the Cmax and AUC of Moexipril decrease by approximately 70% and 40%, respectively; after consuming a high-fat breakfast, the Cmax and AUC decrease by approximately 80% and 50%, respectively. Moexiprilat is excreted via the kidneys. 183 L 441 mL/min

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Metabolism/Metabolite It is rapidly converted to the active metabolite, Moexiprilat. Conversion to the active metabolite is thought to require carboxylesterase, and may occur in organs or tissues other than the gastrointestinal tract where carboxylesterase is present. The liver is considered one site of conversion, but not the primary site.

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Biological Half-Life The elimination half-life of Moexipril is approximately 1 hour. Moexiprila has an elimination half-life of 2 to 9 hours.

Hepatotoxicity
As with other ACE inhibitors, Moexipril is associated with a low incidence of elevated serum transaminases (probability score: E (unlikely, but suspected as a rare cause of clinically significant liver injury)). Pregnancy and Lactation Effects ◉ Overview of Use During Lactation Since there is no information available regarding the use of Moexipril during lactation, alternative medications may be preferred, especially in breastfed newborns or preterm infants. ◉ Effects on Breastfed Infants No relevant published information was found as of the revision date. ◉ Effects on Lactation and Breast Milk No relevant published information was found as of the revision date. Protein Binding The protein binding rate of Moexipril is approximately 50%.

[1]. Chrysant, S.G. and G.S. Chrysant, Pharmacological and clinical profile of moexipril: a concise review. J Clin Pharmacol, 2004. 44(8): p. 827-36.

[2]. Pharmacological and toxicological studies of the new angiotensin converting enzyme inhibitor moexipril hydrochloride. Arzneimittelforschung. 1997 Feb. 47(2):132-44.

[3]. Moexipril, a new angiotensin-converting enzyme (ACE) inhibitor: pharmacological characterization and comparison with enalapril. J Pharmacol Exp Ther. 1995 Nov;275(2):854-63.

[4]. Enalapril and moexipril protect from free radical-induced neuronal damage in vitro and reduce ischemic brain injury in mice and rats. Eur J Pharmacol. 1999 May 28;373(1):21-33.

Moexipril is a peptide drug. Moexipril is a prodrug of the active angiotensin-converting enzyme (ACE) inhibitor Moexiprilat and contains no sulfhydryl group. It is used to treat hypertension. Its mechanism of action is by relaxing blood vessels, causing them to dilate. Lowering high blood pressure helps prevent stroke, heart attack, and kidney disease. Moexipril is an angiotensin-converting enzyme inhibitor. The mechanism of action of Moexipril is as an angiotensin-converting enzyme inhibitor. Moexipril is an angiotensin-converting enzyme (ACE) inhibitor used to treat hypertension. Moexipril is associated with a low incidence of transient elevations in serum transaminases, but has not been found to be associated with cases of acute liver injury. Moexipril is a sulfhydryl-free angiotensin-converting enzyme (ACE) inhibitor with antihypertensive activity. As a prodrug, Moexipril is hydrolyzed to its active form, Moexiprilat, which competitively inhibits angiotensin-converting enzyme (ACE), thereby blocking the conversion of angiotensin I to angiotensin II. This inhibits the action of the potent vasoconstrictor angiotensin II, leading to vasodilation. It also inhibits the adrenal cortex's secretion of angiotensin II-induced aldosterone, thereby promoting diuresis and sodium excretion.
See also: hydrochlorothiazide; Moexipril hydrochloride (note moved to).
Indications
For the treatment of hypertension.
Mechanism of Action
Moexipril is a prodrug of Moexipril, which inhibits angiotensin-converting enzyme (ACE) in humans and animals. The mechanism by which Moexipril lowers blood pressure is thought to be primarily through the inhibition of angiotensin-converting enzyme (ACE) activity. Angiotensin-converting enzyme (ACE) is a peptidyl dipeptidase that catalyzes the conversion of inactive decapeptide angiotensin I into the vasoconstrictor angiotensin II. Angiotensin II is a potent peripheral vasoconstrictor that also stimulates the adrenal cortex to secrete aldosterone and has a negative feedback effect on renin secretion. ACE is the same as kallikrein II, an enzyme that degrades bradykinin (an endothelium-dependent vasodilator). Moexiprila is approximately 1000 times more potent than Moexiprila in inhibiting ACE and kallikrein II. ACE inhibition leads to reduced angiotensin II production, which in turn results in decreased vasoconstriction, increased plasma renin activity, and decreased aldosterone secretion. The latter leads to increased diuresis and sodium excretion, as well as a slight increase in serum potassium concentration (an average increase of approximately 0.25 mEq/L when Moexiprila is used alone). Whether the increased bradykinin (a potent vasodilator) levels play a role in the therapeutic effect of Moexiprila remains to be elucidated. Although the main mechanism by which Moexiprila lowers blood pressure is thought to be through the renin-angiotensin-aldosterone system, ACE inhibitors have some effect on blood pressure even in hypertension with apparent low renin levels.

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Pharmacodynamics
Moexiprila is a non-thiol precursor of the active angiotensin-converting enzyme (ACE) inhibitor Moexiprila. It is used to treat hypertension.
Its mechanism of action is to relax blood vessels, causing them to dilate. Lowering high blood pressure helps prevent stroke, heart attack, and kidney disease.

C27H34N2O7

498.56806

498.236

103775-10-6

Moexipril hydrochloride;82586-52-5;Moexipril-d5;1356929-49-1

91270

Typically exists as solid at room temperature

1.2±0.1 g/cm3

709.3±60.0 °C at 760 mmHg

382.8±32.9 °C

0.0±2.4 mmHg at 25°C

1.565

4.05

2

8

12

36

742

3

CCOC([C@@H](N[C@H](C(N1CC2=CC(=C(C=C2C[C@H]1C(=O)O)OC)OC)=O)C)CCC1C=CC=CC=1)=O

UWWDHYUMIORJTA-HSQYWUDLSA-N

InChI=1S/C27H34N2O7/c1-5-36-27(33)21(12-11-18-9-7-6-8-10-18)28-17(2)25(30)29-16-20-15-24(35-4)23(34-3)14-19(20)13-22(29)26(31)32/h6-10,14-15,17,21-22,28H,5,11-13,16H2,1-4H3,(H,31,32)/t17-,21-,22-/m0/s1

(3S)-2-[(2S)-2-[[(2S)-1-ethoxy-1-oxo-4-phenylbutan-2-yl]amino]propanoyl]-6,7-dimethoxy-3,4-dihydro-1H-isoquinoline-3-carboxylic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

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

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.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*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).

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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)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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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).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)