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Drug-Target Interaction

Drug

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PubChem ID:4501
Structure:
Synonyms:
(1,3)Benzodioxolo(5,6-c)phenanthridinium, 2,3-dimethoxy-12-methyl-
13063-04-2
13063-04-2 (CHLORIDE)
2,3-Dimethoxy-12-methyl-9H-phenanthridino[4',3'-2,1]benzo[4,5-d]1,3-dioxol
2,3-Dimethoxy-12-methyl-9H-phenanthridino[4',3'-2,1]benzo[4,5-d]1,3-dioxolane
2,3-dimethoxy-12-methyl-[1,3]benzodioxolo[5,6-c]phenanthridin-12-ium
6872-57-7
70465-55-3
AC1L1IB4
AC1Q701O
AIDS-003023
AIDS-108185
AIDS003023
AIDS108185
Ambap13063-04-2
Ambap890
AR-1A0300
Benzophenanthridine alkaloid
C09595
CCG-35985
KST-1A7705
NCI60_000995
NCIMech_000542
Neuro_000081
Nitidine
Nitidine chloride
NSC 146397
NSC146397
ZINC00898732

Target

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Uniprot ID:Q6P9U7_RAT
Synonyms:
L-lactate dehydrogenase
EC-Numbers:1.1.1.27
Organism:Rat
Rattus norvegicus
PDB IDs:-

Binding Affinities:

Ki: Kd:Ic 50:Ec50/Ic50:
----

References:

10603424
Protein kinase C inhibitors abolish the increased resistance of diabetic rat heart to ischemia-reperfusion injury.. C H Moon; Y S Jung; S H Lee; E J Baik (1999) The Japanese journal of physiology display abstract
Protein kinase C (PKC) has been implicated in ischemic preconditioning, but whether it plays a role in the cardioprotection observed in the diabetic heart is not known. We assessed the possible role of PKC by investigating whether the inhibition of PKC with staurosporine (Stau, 0.01 microM) or chelerythrine (Chel, 1 microM) can abolish the increased resistance to ischemia (25 min)-reperfusion (30 min) injury in Langendorff perfused hearts from streptozotocin-induced 4-week diabetic rats. In the diabetic heart, pre-ischemic left ventricular developed pressure (LVDP), double product (DP: LVDPxheart rate/1,000), +/- dP/dt(max) and coronary flow rate (CFR) were all reduced compared to the control. The pretreatment with Stau or Chel significantly improved these parameters. The post-ischemic contractile function was recovered to a greater extent in the diabetic heart (116.9 +/- 20.5% of pre-ischemic DP) than in the control (23.3 +/- 2.3% of pre-ischemic DP), indicating the increased resistance of the diabetic heart to ischemia-reperfusion injury. The treatment with Stau or Chel abolished the enhanced recovery in the diabetic heart (36.0 +/- 14.6 and 54.1 +/- 12.8% of pre-ischemic DP, respectively). The reduction in post-ischemic end diastolic pressure (EDP) and lactate dehydrogenase (LDH) release in diabetes (13.5 +/- 2.5 mmHg and 27.2 +/- 6.2 U/g heart) compared to the control (55.8 +/- 2.9 mmHg and 60. 3 +/- 5.7 U/g heart) was significantly (p