Compounds > gap 134
Page last updated: 2024-11-12

gap 134

Description Research Excerpts Clinical Trials Roles Classes Pathways Study Profile Bioassays Related Drugs Related Conditions Protein Interactions Research Growth Market Indicators

Description

danegaptide: an antiarrhythmia agent with cytoprotective activity [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID16656685
CHEMBL ID560592
CHEBI ID177853
SCHEMBL ID2399763
MeSH IDM0536686

Synonyms (36)

Synonym
danegaptide
(2s,4r)-1-(2-aminoacetyl)-4-benzamidopyrrolidine-2-carboxylic acid
CHEBI:177853
943134-39-2
zp1609
CHEMBL560592
zp-1609
gap-134
D09599
danegaptide (usan/inn)
unii-pa0y7735at
pa0y7735at ,
glycyl-(4r)-4-(benzoylamino)-l-proline
danegaptide [usan:inn]
l-proline, glycyl-4-(benzoylamino)-, (4r)-
HY-10913
CS-1100
(2s,4r)-1-(aminoacetyl)-4-(benzoylamino)pyrrolidine-2-carboxylic acid
danegaptide [inn]
danegaptide [usan]
danegaptide [who-dd]
(2s4r)1-(2-amino-acetyl)-4-benzoylamino-pyrrolidine-2-carboxylic acid
(2s,4r) 1-(2-amino-acetyl)-4-benzoylamino-pyrrolidine-2-carboxylic acid
(2s4r) 1-(2-amino-acetyl)-4-benzoylamino-pyrrolidine-2-carboxylic acid
BIZKIHUJGMSVFD-MNOVXSKESA-N
SCHEMBL2399763
AKOS030527026
[2s,4r]-1-(2-aminoacetyl)-4-benzamidopyrrolidine-2-carboxylic acid
DB11821
gap-134;zp 1609
Q27286426
D95155
A917262
943134-39-2 (free base)
(2s,4r)-4-benzamido-1-glycylpyrrolidine-2-carboxylic acid
DTXSID201026039

Research Excerpts

Bioavailability

ExcerptReferenceRelevance
"In an effort to discover potent, orally bioavailable compounds for the treatment of atrial fibrillation (AF) and ventricular tachycardia (VT), we developed a class of gap-junction modifiers typified by GAP-134 (1, R(1)=OH, R(2)=NH(2)), a compound currently under clinical evaluation."( Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
Butera, JA; Di, L; Hennan, JK; Huselton, C; Larsen, BD; Morgan, GA; Piatnitski Chekler, EL; Rossman, EI; Swillo, RE, 2009)		0.35
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Drug Classes (1)

ClassDescription
dipeptideAny molecule that contains two amino-acid residues connected by peptide linkages.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Bioassays (19)

Assay IDTitleYearJournalArticle
AID430410Oral bioavailability in dog at 5 mg/kg2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
AID430391Clearance in CD1 mouse at 0.77 mg/kg, iv2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
AID430310Stability in rat plasma after 3 hrs2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
AID430408Volume of distribution at steady state in dog at 1 mg/kg, iv2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
AID430382Antiarrhythmic activity in calcium chloride-induced mouse arrhythmia model assessed as prolongation of time to conduct cardiac block at 20 pmol/kg, iv relative to control2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
AID430398AUC in CD1 mouse at 0.77 mg/kg, po2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
AID430396Cmax in CD1 mouse at 0.77 mg/kg, po2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
AID430397Tmax in CD1 mouse at 0.77 mg/kg, po2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
AID430392Volume of distribution at steady state in CD1 mouse at 0.77 mg/kg, iv2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
AID430411Half life in dog at 5 mg/kg, po2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
AID430409Half life in dog at 1 mg/kg, iv2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
AID430414AUC in dog at 5 mg/kg, po2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
AID430393Half life in CD1 mouse at 0.77 mg/kg, iv2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
AID430412Cmax in dog at 5 mg/kg, po2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
AID430407Clearance in dog at 1 mg/kg, iv2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
AID430309Antiarrhythmic activity in calcium chloride-induced mouse arrhythmia model assessed as prolongation of time to conduct cardiac block at 10 pmol/kg, iv relative to control2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
AID430394Oral bioavailability in CD1 mouse at 0.77 mg/kg2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
AID430413Tmax in dog at 5 mg/kg, po2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
AID430395Half life in CD1 mouse at 0.77 mg/kg, po2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
Discovery of a class of potent gap-junction modifiers as novel antiarrhythmic agents.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (11)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's0 (0.00)18.2507
2000's1 (9.09)29.6817
2010's8 (72.73)24.3611
2020's2 (18.18)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 30.89

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be moderate demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index30.89 (24.57)
Research Supply Index2.56 (2.92)
Research Growth Index5.63 (4.65)
Search Engine Demand Index53.49 (26.88)
Search Engine Supply Index3.00 (0.95)

This Compound (30.89)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials1 (9.09%)5.53%
Reviews0 (0.00%)6.00%
Case Studies0 (0.00%)4.05%
Observational0 (0.00%)0.25%
Other10 (90.91%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]
ConditionIndicatedRelationship StrengthStudiesTrials
Arrhythmia
[description not available]		02.0510
Auricular Fibrillation
[description not available]		02.0510
Disease Models, Animal
Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases.		02.4820
Atrioventricular Nodal Re-Entrant Tachycardia
[description not available]		02.0510
Arrhythmias, Cardiac
Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.		14.0510
Atrial Fibrillation
Abnormal cardiac rhythm that is characterized by rapid, uncoordinated firing of electrical impulses in the upper chambers of the heart (HEART ATRIA). In such case, blood cannot be effectively pumped into the lower chambers of the heart (HEART VENTRICLES). It is caused by abnormal impulse generation.		02.0510
Tachycardia, Ventricular
An abnormally rapid ventricular rhythm usually in excess of 150 beats per minute. It is generated within the ventricle below the BUNDLE OF HIS, either as autonomic impulse formation or reentrant impulse conduction. Depending on the etiology, onset of ventricular tachycardia can be paroxysmal (sudden) or nonparoxysmal, its wide QRS complexes can be uniform or polymorphic, and the ventricular beating may be independent of the atrial beating (AV dissociation).		02.0510
Cerebral Infarction, Middle Cerebral Artery
[description not available]		02.2510
Cerebral Ischemia
[description not available]		02.2510
Injury, Ischemia-Reperfusion
[description not available]		02.8730
Brain Ischemia
Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). Prolonged ischemia is associated with BRAIN INFARCTION.		02.2510
Reperfusion Injury
Adverse functional, metabolic, or structural changes in tissues that result from the restoration of blood flow to the tissue (REPERFUSION) following ISCHEMIA.		02.8730
Infarction, Middle Cerebral Artery
NECROSIS occurring in the MIDDLE CEREBRAL ARTERY distribution system which brings blood to the entire lateral aspects of each CEREBRAL HEMISPHERE. Clinical signs include impaired cognition; APHASIA; AGRAPHIA; weak and numbness in the face and arms, contralaterally or bilaterally depending on the infarction.		02.2510
Chronic Kidney Diseases
[description not available]		02.3110
Renal Insufficiency, Chronic
Conditions in which the KIDNEYS perform below the normal level for more than three months. Chronic kidney insufficiency is classified by five stages according to the decline in GLOMERULAR FILTRATION RATE and the degree of kidney damage (as measured by the level of PROTEINURIA). The most severe form is the end-stage renal disease (CHRONIC KIDNEY FAILURE). (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002)		02.3110
Ischemia
A hypoperfusion of the BLOOD through an organ or tissue caused by a PATHOLOGIC CONSTRICTION or obstruction of its BLOOD VESSELS, or an absence of BLOOD CIRCULATION.		02.1510
Apoplexy
[description not available]		02.1710
Stroke
A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)		02.1710
ST Elevated Myocardial Infarction
[description not available]		04.8821
Cardiovascular Stroke
[description not available]		02.5220
ST Elevation Myocardial Infarction
A clinical syndrome defined by MYOCARDIAL ISCHEMIA symptoms; persistent elevation in the ST segments of the ELECTROCARDIOGRAM; and release of BIOMARKERS of myocardial NECROSIS (e.g., elevated TROPONIN levels). ST segment elevation in the ECG is often used in determining the treatment protocol (see also NON-ST ELEVATION MYOCARDIAL INFARCTION).		16.8821
Myocardial Infarction
NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).		02.5220
Injury, Myocardial Reperfusion
[description not available]		04.8321