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83915-83-7 molecular structure
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(2S)-1-[(2S)-6-amino-2-{[(1S)-1-carboxy-3-phenylpropyl]amino}hexanoyl]pyrrolidine-2-carboxylic acid

ChemBase ID: 603
Molecular Formular: C21H31N3O5
Molecular Mass: 405.48794
Monoisotopic Mass: 405.22637111
SMILES and InChIs

SMILES:
O=C(N1[C@@H](CCC1)C(=O)O)[C@@H](N[C@@H](CCc1ccccc1)C(=O)O)CCCCN
Canonical SMILES:
NCCCC[C@@H](C(=O)N1CCC[C@H]1C(=O)O)N[C@H](C(=O)O)CCc1ccccc1
InChI:
InChI=1S/C21H31N3O5/c22-13-5-4-9-16(19(25)24-14-6-10-18(24)21(28)29)23-17(20(26)27)12-11-15-7-2-1-3-8-15/h1-3,7-8,16-18,23H,4-6,9-14,22H2,(H,26,27)(H,28,29)/t16-,17-,18-/m0/s1
InChIKey:
RLAWWYSOJDYHDC-BZSNNMDCSA-N

Cite this record

CBID:603 http://www.chembase.cn/molecule-603.html

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NAMES AND DATABASE IDS

NAMES AND DATABASE IDS

Names Database IDs
IUPAC name
(2S)-1-[(2S)-6-amino-2-{[(1S)-1-carboxy-3-phenylpropyl]amino}hexanoyl]pyrrolidine-2-carboxylic acid
IUPAC Traditional name
lisinopril
(2S)-1-[(2S)-6-amino-2-{[(1S)-1-carboxy-3-phenylpropyl]amino}hexanoyl]pyrrolidine-2-carboxylic acid
Brand Name
Acercomp
Inhibril
Linopril
Lisinopril Dihydrate
Lisipril
Lysinopril
Noperten
Presiten
Prinivil
Sinopril
Zestril
Synonyms
Lisinopril
(S)-1-((S)-6-amino-2-(((S)-1-carboxy-3-phenylpropyl)amino)hexanoyl)pyrrolidine-2-carboxylic acid
Acecomb
Acerbon
Acercomp
Alapril
Carace
Coric
Longes
Novatec
Novazyd
Prinivil
Prinzide
Vivatec
Zestoretic
Zestril
Lisinopril
CAS Number
83915-83-7
76547-98-3
PubChem SID
160964066
46504893
PubChem CID
5362119

DATA SOURCES

DATA SOURCES

All Sources Commercial Sources Non-commercial Sources

CALCULATED PROPERTIES

CALCULATED PROPERTIES

JChem ALOGPS 2.1
Acid pKa 3.1725657  H Acceptors
H Donor LogD (pH = 5.5) -3.1054642 
LogD (pH = 7.4) -3.1834292  Log P -3.1026032 
Molar Refractivity 107.3691 cm3 Polarizability 42.540714 Å3
Polar Surface Area 132.96 Å2 Rotatable Bonds 12 
Lipinski's Rule of Five true 
Log P -1.23  LOG S -3.27 
Solubility (Water) 2.16e-01 g/l 

PROPERTIES

PROPERTIES

Physical Property Pharmacology Properties Product Information Bioassay(PubChem)
Solubility
13 mg/L expand Show data source
Hydrophobicity(logP)
-0.9 expand Show data source
Mechanism of Action
ACE inhibitor expand Show data source
Angiotensin antagonist expand Show data source
Description
Conformers expand Show data source
Application(s)
Antihypertensive agent expand Show data source

DETAILS

DETAILS

DrugBank DrugBank
DrugBank - DB00722 external link
Item Information
Drug Groups approved; investigational
Description Lisinopril is a potent, competitive inhibitor of angiotensin-converting enzyme (ACE), the enzyme responsible for the conversion of angiotensin I (ATI) to angiotensin II (ATII). ATII regulates blood pressure and is a key component of the renin-angiotensin-aldosterone system (RAAS). Lisinopril may be used to treat hypertension and symptomatic congestive heart failure, to improve survival in certain individuals following myocardial infarction, and to prevent progression of renal disease in hypertensive patients with diabetes mellitus and microalbuminuria or overt nephropathy.
Indication For the treatment of hypertension and symptomatic congestive heart failure. May be used in conjunction with thrombolytic agents, aspirin and/or β-blockers to improve survival in hemodynamically stable individuals following myocardial infarction. May be used to slow the progression of renal disease in hypertensive patients with diabetes mellitus and microalbuminuria or overt nephropathy.
Pharmacology Lisinopril is an orally active ACE inhibitor that antagonizes the effect 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 using 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 lisinopril by causing increased vasodilation and decreased blood pressure.
Toxicity Symptoms of overdose include severe hypotension, electrolyte disturbances, and renal failure. LD50= 2000 mg/kg(orally in rat). Most frequent adverse effects include headache, dizziness, cough, fatigue and diarrhea.
Affected Organisms
Humans and other mammals
Biotransformation Does not undergo metabolism, excreted unchanged in urine.
Absorption Approximately 25%, but widely variable between individuals (6 to 60%) in all doses tested (5-80 mg); absorption is unaffected by food
Half Life Effective half life of accumulation following multiple dosing is 12 hours.
Protein Binding Lisinopril does not appear to be bound to serum proteins other than ACE.
Elimination Lisinopril does not undergo metabolism and is excreted unchanged entirely in the urine.
Clearance * 10 L/h [child weighting 30 kg receiving doses of 0.1 to 0.2 mg/kg]
References
Abdelmalek MF, Douglas DD: Lisinopril-induced isolated visceral angioedema: review of ACE-inhibitor-induced small bowel angioedema. Dig Dis Sci. 1997 Apr;42(4):847-50. [Pubmed]
Hasslacher C: Influence of the ACE inhibitor lisinopril on blood pressure, metabolism, and renal function parameter in hypertensive type II diabetic patients: a postmarketing surveillance study. J Diabetes Complications. 1996 May-Jun;10(3):136-8. [Pubmed]
Nielsen SE, Sugaya T, Tarnow L, Lajer M, Schjoedt KJ, Astrup AS, Baba T, Parving HH, Rossing P: Tubular and glomerular injury in diabetes and the impact of ACE inhibition. Diabetes Care. 2009 Sep;32(9):1684-8. Epub 2009 Jun 5. [Pubmed]
Patchett AA, Harris E, Tristram EW, Wyvratt MJ, Wu MT, Taub D, Peterson ER, Ikeler TJ, ten Broeke J, Payne LG, Ondeyka DL, Thorsett ED, Greenlee WJ, Lohr NS, Hoffsommer RD, Joshua H, Ruyle WV, Rothrock JW, Aster SD, Maycock AL, Robinson FM, Hirschmann R, Sweet CS, Ulm EH, Gross DM, Vassil TC, Stone CA: A new class of angiotensin-converting enzyme inhibitors. Nature. 1980 Nov 20;288(5788):280-3. [Pubmed]
External Links
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Drugs.com

REFERENCES

REFERENCES

From Suppliers Google Scholar IconGoogle Scholar PubMed iconPubMed Google Books IconGoogle Books
  • • Abdelmalek MF, Douglas DD: Lisinopril-induced isolated visceral angioedema: review of ACE-inhibitor-induced small bowel angioedema. Dig Dis Sci. 1997 Apr;42(4):847-50. Pubmed
  • • Hasslacher C: Influence of the ACE inhibitor lisinopril on blood pressure, metabolism, and renal function parameter in hypertensive type II diabetic patients: a postmarketing surveillance study. J Diabetes Complications. 1996 May-Jun;10(3):136-8. Pubmed
  • • Nielsen SE, Sugaya T, Tarnow L, Lajer M, Schjoedt KJ, Astrup AS, Baba T, Parving HH, Rossing P: Tubular and glomerular injury in diabetes and the impact of ACE inhibition. Diabetes Care. 2009 Sep;32(9):1684-8. Epub 2009 Jun 5. Pubmed
  • • Patchett AA, Harris E, Tristram EW, Wyvratt MJ, Wu MT, Taub D, Peterson ER, Ikeler TJ, ten Broeke J, Payne LG, Ondeyka DL, Thorsett ED, Greenlee WJ, Lohr NS, Hoffsommer RD, Joshua H, Ruyle WV, Rothrock JW, Aster SD, Maycock AL, Robinson FM, Hirschmann R, Sweet CS, Ulm EH, Gross DM, Vassil TC, Stone CA: A new class of angiotensin-converting enzyme inhibitors. Nature. 1980 Nov 20;288(5788):280-3. Pubmed
  • • Eur. Pat., 1980, Merck, 12 401; CA, 95, 25634j, (synth, pharmacol)
  • • Brunner, D.B. et al., Br. J. Clin. Pharmacol., 1981, 11, 461, (pharmacol)
  • • Derkx, F.H.M. et al., Prog. Pharmacol., 1984, 5, 93, (pharmacol)
  • • Wu, M.T. et al., J. Pharm. Sci., 1985, 74, 352, (synth)
  • • Noble, T.A. et al., Clin. Pharm., 1988, 7, 659, (rev)
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  • • Ip, D.P. et al., Anal. Profiles Drug Subst., 1992, 21, 233, (rev)
  • • Patchett, A.A., Chron. Drug Discovery, 1993, 3, 125, (rev)
  • • Negwer, M., Organic-Chemical Drugs and their Synonyms, 7th edn., Akademie-Verlag, 1994, 8692, (synonyms)
  • • ACE Inhibitors: Current Use and Future Prospects, (Ed. Schachter, M.), M. Dunitz, London, 1995, (book)
  • • Droste, H.T. et al., Neth. J. Med., 1995, 46, 95, (tox)
  • • Goa, K.L. et al., Drugs, 1996, 52, 564; 1997, 53, 1081-1105, (rev)
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