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 incompletely absorbed, with bioavailability as moexiprilat of about 13% compared to intravenous (I.V.) moexipril (both measuring the metabolite moexiprilat), and is markedly affected by food, which reduces Cmax and AUC by about 70% and 40%, respectively, after the ingestion of a low-fat breakfast or by 80% and 50%, respectively, after the ingestion of a high-fat breakfast.
Moexiprilat undergoes renal elimination.
183 L
441 mL/min

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Metabolism / Metabolites
Rapidly converted to moexiprilat, the active metabolite. Conversion to the active metabolite is thought to require carboxyesterases and is likely to occur in organs or tissues, other than the gastrointestinal tract, in which carboxyesterases occur. The liver is thought to be one site of conversion, but not the primary site.

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Biological Half-Life
Moexipril elimination half-life is approximately 1 hour. Moexiprilat elimination half-life is 2 to 9 hours.

Hepatotoxicity
Moexipril, like other ACE inhibitors, is associated with a low rate of serum aminotransferase elevations (
Likelihood score: E* (unlikely but suspected rare cause of clinically apparent liver injury).

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Because no information is available on the use of moexipril during breastfeeding, an alternate drug may be preferred, especially while nursing a newborn or preterm infant.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Protein Binding
Moexiprilat is approxomately 50% protein bound.

[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.
Moexipril is a non-sulfhydryl containing precursor of the active angiotensin-converting enzyme (ACE) inhibitor moexiprilat. It is used to treat high blood pressure (hypertension). It works by relaxing blood vessels, causing them to widen. Lowering high blood pressure helps prevent strokes, heart attacks and kidney problems.
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 which is used in the therapy of hypertension. Moexipril is associated with a low rate of transient serum aminotransferase elevations, but has yet to be linked to instances of acute liver injury.
Moexipril is a non-sulfhydryl angiotensin converting enzyme (ACE) inhibitor with antihypertensive activity. As a prodrug, moexipril is hydrolyzed into its active form moexiprilat, which competitively inhibits ACE, thereby blocking the conversion of angiotensin I to angiotensin II. This prevents the actions of the potent vasoconstrictor angiotensin II and leads to vasodilation. It also prevents angiotensin II-induced aldosterone secretion by the adrenal cortex, thereby promoting diuresis and natriuresis.
See also: Hydrochlorothiazide; moexipril hydrochloride (annotation moved to).

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Drug Indication
For the treatment of hypertension.

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Mechanism of Action
Moexipril is a prodrug for moexiprilat, which inhibits ACE in humans and animals. The mechanism through which moexiprilat lowers blood pressure is believed to be primarily inhibition of ACE activity. ACE is a peptidyl dipeptidase that catalyzes the conversion of the inactive decapeptide angiotensin I to the vasoconstrictor substance angiotensin II. Angiotensin II is a potent peripheral vasoconstrictor that also stimulates aldosterone secretion by the adrenal cortex and provides negative feedback on renin secretion. ACE is identical to kininase II, an enzyme that degrades bradykinin, an endothelium-dependent vasodilator. Moexiprilat is about 1000 times as potent as moexipril in inhibiting ACE and kininase II. Inhibition of ACE results in decreased angiotensin II formation, leading to decreased vasoconstriction, increased plasma renin activity, and decreased aldosterone secretion. The latter results in diuresis and natriuresis and a small increase in serum potassium concentration (mean increases of about 0.25 mEq/L were seen when moexipril was used alone). Whether increased levels of bradykinin, a potent vasodepressor peptide, play a role in the therapeutic effects of moexipril remains to be elucidated. Although the principal mechanism of moexipril in blood pressure reduction is believed to be through the renin-angiotensin-aldosterone system, ACE inhibitors have some effect on blood pressure even in apparent low-renin hypertension.

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Pharmacodynamics
Moexipril is a non-sulfhydryl containing precursor of the active angiotensin-converting enzyme (ACE) inhibitor moexiprilat. It is used to treat high blood pressure (hypertension). It works by relaxing blood vessels, causing them to widen. Lowering high blood pressure helps prevent strokes, heart attacks and kidney problems.

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.)