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Drug-Target Interaction

Drug

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PubChem ID:5278
Structure:
Synonyms:
1-Phthalazineacetic acid,
1-Phthalazineacetic acid, 3-((4-bromo-2-fluorophenyl)methyl)-3,4-dihydro-4-oxo-
3-(4-Bromo-2-fluorobenzyl)-3,4-dihydro-4-oxo-1-phthalazineacetic acid
3-(4-bromo-2-fluorobenzyl)-3,4-dihydro-4-oxo-3H-phthalazin-1-ylacetic acid
3-(4-bromo-2-fluorobenzyl)-4-oxo-3h-phthalazin-1-ylacetic acid
72702-95-5
Bio1_000383
Bio1_000872
Bio1_001361
BSPBio_002576
C17H12BrFN2O3
D03806
DivK1c_006939
ICI 128,436
ICI 128436
ICI-128436
KBio1_001883
KBio2_001963
KBio2_004531
KBio2_007099
KBio3_001796
KBioGR_001855
KBioSS_001963
LS-176986
MK-538
NCGC00024824-01
PONALRESTAT
Ponalrestat (USAN/INN)
Ponalrestat [USAN:BAN:INN]
Ponalrestatum [Latin]
Prodiax
SPBio_001393
SpecPlus_000843
Spectrum2_001467
Spectrum3_001048
Spectrum4_001188
Spectrum_001483
Statil
Tocris-0847

Target

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Uniprot ID:AT1A3_MOUSE
Synonyms:
Na(+)/K(+) ATPase alpha(III) subunit
Na(+)/K(+) ATPase alpha-3 subunit
Sodium pump subunit alpha-3
Sodium/potassium-transporting ATPase subunit alpha-3
EC-Numbers:3.6.3.9
Organism:Mouse
Mus musculus
PDB IDs:-

Binding Affinities:

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

References:

2161366
Coexistence of nerve conduction deficit with increased Na(+)-K(+)-ATPase activity in galactose-fed mice. Implications for polyol pathway and diabetic neuropathy.. N A Calcutt; D R Tomlinson; S Biswas (1990) Diabetes display abstract
We measured motor nerve conduction velocity (MNCV), Na(+)-K(+)-ATPase activity, polyol-pathway metabolites, and myo-inositol in sciatic nerves from control mice, galactose-fed (20% wt/wt diet) mice, and galactose-fed mice given the aldose reductase inhibitor ponalrestat (300-mg/kg diet). Treatments were maintained for 4 wk. Galactose feeding was associated with a 21.5% reduction in MNCV (P less than 0.001), which was almost completely prevented by ponalrestat. Galactose-fed mice showed an 81% increase in Na(+)-K(+)-ATPase (P less than 0.01), an effect completely prevented by aldose reductase inhibition. Treatment of a separate galactose-fed group with sorbinil (300 mg/kg diet) also attenuated the MNCV deficit and prevented the increased Na(+)-K(+)-ATPase activity associated with galactosemia. Accumulation of galactitol in the nerves of galactose-fed mice was prevented by aldose reductase inhibition, but there were no alterations in myo-inositol levels in the sciatic nerves of any group. These data show that exaggerated flux through the polyol pathway can cause an MNCV deficit that is unrelated to either myo-inositol levels or NA(+)-K(+)-ATPase activity.