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Trandolapril (RU44570)

Alias: RU 44570 Mavik RU-44570GoptenRU44570 Odrik
Cat No.:V16691 Purity: ≥98%
Trandolapril(RU-44570; Mavik; Gopten;RU44570; Odrik), an antihypertensive drug, is anoral andnonsulfhydryl prodrug that has to be hydrolysed to the active diacid Trandolaprilat.
Trandolapril (RU44570)
Trandolapril (RU44570) Chemical Structure CAS No.: 87679-37-6
Product category: ACE
This product is for research use only, not for human use. We do not sell to patients.
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50mg
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Other Forms of Trandolapril (RU44570):

  • Trandolapril hydrochloride (RU44570 hydrochloride)
  • Trandolapril D5
Official Supplier of:
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Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Trandolapril (RU-44570; Mavik; Gopten; RU44570; Odrik), an antihypertensive drug, is an oral and nonsulfhydryl prodrug that has to be hydrolysed to the active diacid Trandolaprilat. It is a potent ACE inhibitor used to treat high blood pressure. Trandolapril acts by competitive inhibition of angiotensin converting enzyme (ACE), a key enzyme in the renin-angiotensin system which plays an important role in regulating blood pressure.

Biological Activity I Assay Protocols (From Reference)
ln Vitro
Trandolapril (0.02 mM, 1 mM; 3 d) increases the proportion of apoptotic cells in the K562 cell line by inhibiting cell development and inducing apoptosis [2].
ln Vivo
By limiting renal interstitial matrix expression and myofibroblast activation, as well as lowering renal proinflammatory cytokines RANTES and TNF-α levels in mice with renal fibrosis, trunolapril (3 mg/kg/day; oral; 7 days) decreases obstructive nephropathy in mice [2]. In rats, trundialolapril (0.3 mg/kg/day; oral; 4 weeks) reduces cellular fibronectin accumulation, collagen, and arterial hypertrophy [3]. In rats, long-term antihypertensive effects of landopril (0.3 mg/kg/day; oral; 4 months) lower blood pressure [3]. When given orally, twice daily for four months, trundialapril (0.25 mg/kg) prevents atherosclerosis in rabbits with Watanabe hereditary hyperlipidemia [4].
Cell Assay
Apoptosis analysis [2]
Cell Types: K562, KU812, U937 and HL60
Tested Concentrations: 0-2 mM
Incubation Duration: 0, 1, 2, 3 days
Experimental Results: 1 mM inhibits K562, KU812, U937, 0.02 mM inhibits HL60.
Animal Protocol
Animal/Disease Models: UUD (unilateral ureteral obstruction) model [2] in male CD-1 mice (18-22 g)
Doses: 3 mg/kg
Route of Administration: po (oral gavage); one time/day for 7 days
Experimental Results: Caused Renal interstitial matrix expression, including fibronectin, type I and type III collagen, is diminished and, surprisingly, myofibroblast activation is inhibited through α-smooth muscle actin (a-SMA) expression, which reduces RANTES (regulated activation, normal T cell expression and secretion) and TNF-α levels.

Animal/Disease Models: SHR model (spontaneous hypertensive rats, 4 weeks old) [3]
Doses: 0.3 mg/kg
Route of Administration: po (oral gavage); one time/day for 4 weeks
Experimental Results: The collagen content in the aortic middle layer diminished, Arterial distensibility increases by approximately 80%.

Animal/Disease Models: Watanabe hereditary hyperlipidemia rabbit (3 months old) [4]
Doses: 0.25 mg/kg
Route of Administration: po (oral gavage); twice a day; 9-month
Experimental Results: Atherosclerosis on the intimal surface Sclerosis is diminished, and the cholesterol c
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
~ 40-60% absorbed; extensive first pass metabolism results in a low bioavailability of 4-14%
After oral administration of trandolapril, about 33% of parent drug and metabolites are recovered in urine, mostly as trandolaprilat, with about 66% in feces.
18 L
52 L/h [After approximately 2 mg IV doses]
/MILK/ Trandolapril and its metabolites are distributed into milk in rats.
After oral administration of trandolapril, about 33% of parent drug and metabolites are recovered in urine, mostly as trandolaprilat, with about 66% in feces. The extent of the absorbed dose which is biliary excreted has not been determined. Plasma concentrations (Cmax and AUC of trandolapril and Cmax of trandolaprilat) are dose proportional over the 1-4 mg range, but the AUC of trandolaprilat is somewhat less than dose proportional. In addition to trandolaprilat, at least 7 other metabolites have been found, principally glucuronides or deesterification products.
Serum protein binding of trandolapril is about 80%, and is independent of concentration. Binding of trandolaprilat is concentration-dependent, varying from 65% at 1000 ng/mL to 94% at 0.1 ng/mL, indicating saturation of binding with increasing concentration.
Absolute bioavailability after oral administration of trandolapril is about 10% as trandolapril and 70% as trandolaprilat. After oral trandolapril under fasting conditions, peak trandolapril levels occur at about one hour and peak trandolaprilat levels occur between 4 and 10 hours. The elimination half-life of trandolapril is about 6 hours. At steady state, the effective half-life of trandolaprilat is 22.5 hours. Like all ACE inhibitors, trandolaprilat also has a prolonged terminal elimination phase, involving a small fraction of administered drug, probably representing binding to plasma and tissue ACE. During multiple dosing of trandolapril, there is no significant accumulation of trandolaprilat. Food slows absorption of trandolapril, but does not affect AUC or Cmax of trandolaprilat or Cmax of trandolapril.
The volume of distribution of trandolapril is about 18 liters. Total plasma clearances of trandolapril and trandolaprilat after approximately 2 mg IV doses are about 52 liters/hour and 7 liters/hour respectively. Renal clearance of trandolaprilat varies from 1- 4 liters/hour, depending on dose.
Metabolism / Metabolites
Cleavage of the ester group of trandolapril, primarily in the liver, is responsible for conversion to trandolaprilat, the active metabolite. Seven other metabolites, including diketopiperazine and glucuronide conjugated derivatives of trandolapril and trandolaprilat, have been identified.
Trandolapril is a prodrug and has little pharmacologic activity until hydrolyzed in the liver to trandolaprilat.
Trandolapril's angiotensin-converting enzyme (ACE)-inhibiting activity is primarily due to its diacid metabolite, trandolaprilat. Cleavage of the ester group of trandolapril, primarily in the liver, is responsible for conversion.
After oral administration of trandolapril, about 33% of parent drug and metabolites are recovered in urine, mostly as trandolaprilat, with about 66% in feces. ... In addition to trandolaprilat, at least 7 other metabolites have been found, principally glucuronides or deesterification products.
Biological Half-Life
The elimination half lives of trandolapril and trandolaprilat are about 6 and 10 hours, respectively, but, similar to all ACE inhibitors, trandolaprilat also has a prolonged terminal elimination phase that involves a small fraction of administered drug. This likely represents drug binding to plasma and tissue ACE. The effective half life of elimination for trandolaprilat is 16-24 hours.
At steady state, the effective half-life of trandolaprilat is 22.5 hours. /Trandolaprilat/
Toxicity/Toxicokinetics
Toxicity Summary
IDENTIFICATION AND USE: Trandolapril is a colorless, crystalline solid. Trandolapril tablets are indicated for the treatment of hypertension. HUMAN STUDIES: In humans, the most likely clinical manifestation would be symptoms attributable to severe hypotension. Symptoms expected with angiotensin-converting enzyme (ACE) inhibitors are hypotension, hyperkalemia, and renal failure. Rare angiotensin-converting enzyme (ACE) inhibitor-associated clinical syndrome manifested initially by cholestatic jaundice may occur; this may progress to fulminant hepatic necrosis and is potentially fatal. Patients receiving an ACE inhibitor, including trandolapril, who develop jaundice or marked elevations in hepatic enzymes should discontinue the drug and receive appropriate monitoring. Use of drugs that act on the renin-angiotensin system during the second and third trimesters of pregnancy reduces fetal renal function and increases fetal and neonatal morbidity and death. Resulting oligohydramnios can be associated with fetal lung hypoplasia and skeletal deformations. Potential neonatal adverse effects include skull hypoplasia, anuria, hypotension, renal failure, and death. ANIMAL STUDIES: In dogs, an oral dose of 1000 mg/kg did not cause mortality and abnormal clinical signs were not observed. In rats, an oral dose of 5000 mg/kg caused low mortality (1 male out of 5; 0 females). A perinatal and postnatal study was performed in female Sprague-Dawley rats treated orally with trandolapril at dosage levels of 3, 30 and 300 mg/kg/day from day 17 of pregnancy to postpartum day 21. Incidence of dilatation of renal pelvis with higher value in kidney weight was increased in offspring in the 30 and 300 mg/kg dosage groups, and water consumption at the same dosage groups was higher than that of the control group. Body weight gain in offspring was depressed in each treated group and viability of offspring from postpartum day 0 to day 4 was slightly decreased in the 30 and 300 mg/kg dosage groups comparing with that of the control group. No adverse effects were observed on the other postnatal development of the offspring, such as differentiation, sexual maturation, reflex, motor activity, emotionality, learning ability and reproductive performance. No adverse effects were detected in the second generation offspring.
Hepatotoxicity
Trandolapril, like other ACE inhibitors, has been associated with a low rate of serum aminotransferase elevations (
Likelihood score: E* (unproven but suspected rare cause of clinically apparent liver injury).
Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Because no information is available on the use of trandolapril 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.
Protein Binding
Serum protein binding of trandolapril is ~ 80% (independent of concentration and not saturable) while that of trandolaprilat is 65 to 94% (concentration-dependent and saturable).
Interactions
The hypotensive effect of certain inhalation anesthetics may be enhanced by angiotensin-converting enzyme (ACE) inhibitors including trandolapril.
Patients taking concomitant mammalian target of rapamycin (mTOR)inhibitor (e.g., temsirolimus, sirolimus, everolimus) therapy may be at increased risk for angioedema.
Nitritoid reactions (symptoms include facial flushing, nausea, vomiting and hypotension) have been reported rarely in patients on therapy with injectable gold (sodium aurothiomalate) and concomitant angiotensin-converting enzyme (ACE) inhibitor therapy including trandolapril.
In patients who are elderly, volume-depleted (including those on diuretic therapy), or with compromised renal function, co- administration of non-steroidal anti-inflammatory drugs (NSAIDs), including selective cyclooxygenase-2 (COX-2) inhibitors, with angiotensin-converting enzyme (ACE) inhibitors, including trandolapril, may result in deterioration of renal function, including possible acute renal failure. These effects are usually reversible. Monitor renal function periodically in patients receiving trandolapril and NSAID therapy. The antihypertensive effect of ACE inhibitors, including trandolapril may be attenuated by NSAIDs.
For more Interactions (Complete) data for Trandolapril (9 total), please visit the HSDB record page.
Non-Human Toxicity Values
LD50 Mouse (male) oral 4875 mg/kg
LD50 Mouse (female) oral 3990 mg/kg
References

[1]. Trandolapril. An update of its pharmacology and therapeutic use in cardiovascular disorders. Drugs. 1998 Nov;56(5):871-93.

[2]. Combination therapy with paricalcitol and trandolapril reduces renal fibrosis in obstructive nephropathy. Kidney Int. 2009 Dec;76(12):1248-57.

[3]. Prevention of arterial structural alterations with verapamil and trandolapril and consequences for mechanical properties in spontaneously hypertensive rats. Eur J Pharmacol. 1998 Nov 13;361(1):51-60.

[4]. Trandolapril inhibits atherosclerosis in the Watanabe heritable hyperlipidemic rabbit. Hypertension. 1992 Oct;20(4):473-7.

Additional Infomation
Therapeutic Uses
/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Trandolapril is included in the database.
Trandolapril tablets are indicated for the treatment of hypertension. It may be used alone or in combination with other antihypertensive medication such as hydrochlorothiazide. /Included in US product label/
Trandolapril tablets are indicated in stable patients who have evidence of left-ventricular systolic dysfunction (identified by wall motion abnormalities) or who are symptomatic from congestive heart failure within the first few days after sustaining acute myocardial infarction. Administration of trandolapril to Caucasian patients has been shown to decrease the risk of death (principally cardiovascular death) and to decrease the risk of heart failure-related hospitalization. /Included in US product label/
ACE inhibitors have been used in the management of heart failure, usually in conjunction with other agents such as cardiac glycosides, diuretics, and beta-blockers. /Angiotensin-converting enzyme (ACE) inhibitors; NOT included in US product label/
For more Therapeutic Uses (Complete) data for Trandolapril (6 total), please visit the HSDB record page.
Drug Warnings
/BOXED WARNING/ When pregnancy is detected, discontinue trandolapril as soon as possible. Drugs that act directly on the renin-angiotensin system can cause injury and death to the developing fetus.
Angioedema of the face, extremities, lips, tongue, glottis, and larynx has been reported in patients treated with angiotensin-converting enzyme (ACE) inhibitors including trandolapril. Symptoms suggestive of angioedema or facial edema occurred in 0.13% of trandolapril-treated patients. Two of the four cases were life-threatening and resolved without treatment or with medication (corticosteroids). Angioedema associated with laryngeal edema can be fatal. If laryngeal stridor or angioedema of the face, tongue or glottis occurs, treatment with trandolapril should be discontinued immediately, the patient treated in accordance with accepted medical care and carefully observed until the swelling disappears. In instances where swelling is confined to the face and lips, the condition generally resolves without treatment; antihistamines may be useful in relieving symptoms.
Use of drugs that act on the renin-angiotensin system during the second and third trimesters of pregnancy reduces fetal renal function and increases fetal and neonatal morbidity and death. Resulting oligohydramnios can be associated with fetal lung hypoplasia and skeletal deformations. Potential neonatal adverse effects include skull hypoplasia, anuria, hypotension, renal failure, and death. When pregnancy is detected, discontinue trandolapril as soon as possible. These adverse outcomes are usually associated with use of these drugs in the second and third trimester of pregnancy. Most epidemiologic studies examining fetal abnormalities after exposure to antihypertensive use in the first trimester have not distinguished drugs affecting the renin-angiotensin system from other antihypertensive agents. Appropriate management of maternal hypertension during pregnancy is important to optimize outcomes for both mother and fetus. /Angiotensin-converting enzyme (ACE) inhibitors/
Like other angiotensin-converting enzyme (ACE) inhibitors, trandolapril rarely is associated with hypotension in patients with uncomplicated hypertension. Symptomatic hypotension may occur; patients at particular risk include those with severe volume and/or salt depletion secondary to prolonged diuretic therapy, dietary salt restriction, dialysis, diarrhea, or vomiting. Volume and/or salt depletion should be corrected before starting trandolapril therapy. Marked hypotension, which may be associated with oliguria and/or progressive azotemia and rarely with acute renal failure and/or death, may occur in patients with heart failure (with or without associated renal impairment). In patients with heart failure, trandolapril therapy should be started at the recommended dose under close medical supervision with close monitoring for the first 2 weeks of treatment and whenever the dosage of trandolapril or diuretic is increased. Hypotension also should be avoided in patients with ischemic heart disease, aortic stenosis, or cerebrovascular disease.
For more Drug Warnings (Complete) data for Trandolapril (13 total), please visit the HSDB record page.
Pharmacodynamics
Trandolapril is the ethyl ester prodrug of a nonsulfhydryl ACE inhibitor, trandolaprilat. Trandolapril is deesterified in the liver to the diacid metabolite, trandolaprilat, which is approximately eight times more active as an inhibitor of ACE than its parent compound. ACE is a peptidyl dipeptidase that is part of the RAAS. The RAAS is a homeostatic mechanism for regulating hemodynamics, water and electrolyte balance. During sympathetic stimulation or when renal blood pressure or blood flow is reduced, renin is released from the granular cells of the juxtaglomerular apparatus in the kidneys. In the blood stream, renin cleaves circulating angiotensinogen to ATI, which is subsequently cleaved to ATII by ACE. ATII increases blood pressure via a number of mechanisms. First, it stimulates the secretion of aldosterone from the adrenal cortex. Aldosterone travels to the distal convoluted tubule (DCT) and collecting tubule of nephrons where it increases sodium and water reabsorption by increasing the number of sodium channels and sodium-potassium ATPases on cell membranes. Second, ATII stimulates the secretion of vasopressin (also known as antidiuretic hormone or ADH) from the posterior pituitary gland. ADH stimulates further water reabsorption from the kidneys via insertion of aquaporin-2 channels on the apical surface of cells of the DCT and collecting tubules. Third, ATII increases blood pressure through direct arterial vasoconstriction. Stimulation of the Type 1 ATII receptor on vascular smooth muscle cells leads to a cascade of events resulting in myocyte contraction and vasoconstriction. In addition to these major effects, ATII induces the thirst response via stimulation of hypothalamic neurons. ACE inhibitors inhibit the rapid conversion of ATI to ATII and antagonize RAAS-induced increases in blood pressure. ACE (also known as kininase II) is also involved in the enzymatic deactivation of bradykinin, a vasodilator. Inhibiting the deactivation of bradykinin increases bradykinin levels and may further sustain the effects of trandolaprilat by causing increased vasodilation and decreased blood pressure. The blood pressure lowering effect of trandolaprilat is due to a decrease in peripheral vascular resistance, which is not accompanied by significant changes in urinary excretion of chloride or potassium or water or sodium retention.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C24H34N2O5
Molecular Weight
430.54
Exact Mass
430.246
CAS #
87679-37-6
Related CAS #
Trandolapril hydrochloride;87725-72-2;Trandolapril-d5;1356847-98-7
PubChem CID
5484727
Appearance
White to off-white solid powder
Density
1.2±0.1 g/cm3
Boiling Point
626.0±55.0 °C at 760 mmHg
Melting Point
122-123°C
Flash Point
332.4±31.5 °C
Vapour Pressure
0.0±1.9 mmHg at 25°C
Index of Refraction
1.549
LogP
3.97
Hydrogen Bond Donor Count
2
Hydrogen Bond Acceptor Count
6
Rotatable Bond Count
10
Heavy Atom Count
31
Complexity
634
Defined Atom Stereocenter Count
5
SMILES
CCOC(=O)[C@H](CCC1=CC=CC=C1)N[C@@H](C)C(=O)N2[C@H]3CCCC[C@@H]3C[C@H]2C(=O)O
InChi Key
VXFJYXUZANRPDJ-WTNASJBWSA-N
InChi Code
InChI=1S/C24H34N2O5/c1-3-31-24(30)19(14-13-17-9-5-4-6-10-17)25-16(2)22(27)26-20-12-8-7-11-18(20)15-21(26)23(28)29/h4-6,9-10,16,18-21,25H,3,7-8,11-15H2,1-2H3,(H,28,29)/t16-,18+,19-,20-,21-/m0/s1
Chemical Name
(2S,3aR,7aS)-1-[(2S)-2-[[(2S)-1-ethoxy-1-oxo-4-phenylbutan-2-yl]amino]propanoyl]-2,3,3a,4,5,6,7,7a-octahydroindole-2-carboxylic acid
Synonyms
RU 44570 Mavik RU-44570GoptenRU44570 Odrik
HS Tariff Code
2934.99.9001
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)
Solubility Data
Solubility (In Vitro)
DMSO : ~100 mg/mL (~232.27 mM)
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.08 mg/mL (4.83 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 (4.83 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.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (4.83 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (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 corn oil and mix evenly.


 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 2.3227 mL 11.6133 mL 23.2266 mL
5 mM 0.4645 mL 2.3227 mL 4.6453 mL
10 mM 0.2323 mL 1.1613 mL 2.3227 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.

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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.

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