(7- (5- fluoro- 2- methylphenyl)- 4- methyl- 7,8- dihydro- 5(6H)- quinolinylideneamino)guanidine

an inhibitor of Na(+)/H(+)-exchanger isoform NHE1; structure in first source

Also Known As:

(5E,7S)-(7-(5-fluoro-2-methylphenyl)-4-methyl-7,8-dihydro-5(6H)-quinolinylideneamino)guanidine dimethanesulfonate; T 162559

Networked: 2 relevant articles (0 outcomes, 1 trials/studies)

Bio-Agent Context: Research Results

Organic Chemicals: 133
- Amidines: 14
  - Guanidines: 29
    - (7-(5-fluoro-2-methylphenyl)-4-methyl-7,8-dihydro-5(6H)-quinolinylideneamino)guanidine: 2
Heterocyclic Compounds: 198
- Fused-Ring Heterocyclic Compounds
  - 2-Ring Heterocyclic Compounds
    - Quinolines: 146
      - (7-(5-fluoro-2-methylphenyl)-4-methyl-7,8-dihydro-5(6H)-quinolinylideneamino)guanidine: 2

Experts

1.	Haddad, Gabriel G: 1 article (02/2008)
2.	Xue, Jin: 1 article (02/2008)
3.	Yao, Hang: 1 article (02/2008)
4.	Zhou, Dan: 1 article (02/2008)
5.	Abe, Akemi: 1 article (04/2002)
6.	Fukumoto, Shoji: 1 article (04/2002)
7.	Igata, Hideki: 1 article (04/2002)
8.	Ikeda, Shota: 1 article (04/2002)
9.	Imamiya, Eikoh: 1 article (04/2002)
10.	Kusumoto, Keiji: 1 article (04/2002)

Related Diseases

1.	Hypoxia (Hypoxemia) 02/01/2008 - "Pharmacological studies revealed 1) no significant difference in neuronal injury between controls (no inhibitor) and inhibition of Na(+)-K(+)-ATP pump, voltage-gated Na(+) channel, ATP-sensitive K(+) channel, or reverse mode of Na(+)/Ca(2+) exchanger under hypoxia; however, 2) inhibition of NBCs with 500 microM DIDS did not cause hypoxic death in either cultured cortical neurons or hippocampal slices; 3) in contrast, inhibition of Na(+)/H(+) exchanger isoform 1 (NHE1) with either 10 microM HOE-642 or 2 microM T-162559 resulted in dramatic hypoxic injury (+95% for HOE-642 and +100% for T-162559 relative to normoxic control, P < 0.001) on treatment day 3, when no death occurred for hypoxic controls (no inhibitor). "
2.	Reperfusion Injury 04/01/2002 - "5. These results indicate that the new structural NHE-1 inhibitor T-162559 is more potent than cariporide and eniporide and possesses a cardioprotective effect against ischaemia and reperfusion injury in rat and rabbit models."
3.	Myocardial Infarction 04/01/2002 - "4. Intravenous administration of T-162559 (0.03 and 0.1 mg kg(-1)) significantly inhibited the progression of myocardial infarction induced by left coronary artery occlusion and reperfusion in rabbits; the infarct size normalized by area at risk was 74+/-6% in the vehicle group, and 47+/-5% and 51+/-7% in the T-162559-0.03 mg kg(-1) and T-162559-0.1 mg kg(-1) groups (both P<0.05), respectively. "
4.	Infarction (Infarctions) 04/01/2002 - "4. Intravenous administration of T-162559 (0.03 and 0.1 mg kg(-1)) significantly inhibited the progression of myocardial infarction induced by left coronary artery occlusion and reperfusion in rabbits; the infarct size normalized by area at risk was 74+/-6% in the vehicle group, and 47+/-5% and 51+/-7% in the T-162559-0.03 mg kg(-1) and T-162559-0.1 mg kg(-1) groups (both P<0.05), respectively. "
5.	Contracture 04/01/2002 - "3. T-162559 inhibited, in a concentration-dependent manner, the reduction in cardiac contractility, progression of cardiac contracture, and increase in lactate dehydrogenase release after global ischaemia and reperfusion in perfused rat hearts. "

Related Drugs and Biologics

1.	cariporide
2.	Protein Isoforms (Isoforms)
3.	Sodium-Calcium Exchanger
4.	Sodium-Hydrogen Exchangers
5.	4,4'- Diisothiocyanostilbene- 2,2'- Disulfonic Acid (DIDS)
6.	Adenosine Triphosphate (ATP)
7.	L-Lactate Dehydrogenase (Lactate Dehydrogenase)
8.	eniporide

Related Therapies and Procedures

1.	Intravenous Administration