Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Chemical Compound Review:

Mozavaptan N-[4-[(2-dimethylamino-6...

Synonyms: CHEMBL420762, Opc-31260, AC-4255, CHEBI:229399, AC1L3OOQ, ...

Yokoi, H. et al., Gattone, V.H. et al., Gattone, V.H. et al., Torres, V.E. et al., Sato, K. et al., et al.

Yokoi, Nagasaki, Tachikawa, Arima, Murase, Miura, Hirabayashi, Oiso, Gattone, Maser, Tian, Rosenberg, Branden, Torres, Wang, Qian, Somlo, Harris, Gattone,

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Disease relevance of Opc 31260

OPC31260 treatment of cystic mice led to an amelioration of the cystic enlargement and azotemia [1].
When diet containing OPC31260 had been provided for 4 days until the day before the start of water loading, antidiuresis and hyponatremia (125.4 +/- 1.mEq/l) were significantly potentiated [2].

Psychiatry related information on Opc 31260

Treatment with OPC31260 (40 mg/kg of weight per d) inhibited up to 20 to 30% the upregulation of AQP-mRNA induced by water deprivation [3].

High impact information on Opc 31260

The vasopressin V2 receptor (VPV2R) antagonist OPC31260 has been effective in two animal models of PKD with pathologies that are probably related [4].
We used animal models orthologous to the human disorders to test whether a vasopressin V2 receptor (VPV2R) antagonist, OPC31260, would be effective against early or established disease [5].
This vasodilatory effect of AVP was abolished by pretreatment with a V2 antagonist, OPC31260 [6].
Furthermore, the AVP-induced AM-LI secretion was blocked by a V2 receptor antagonist (OPC31260), but not by a V1 receptor antagonist (OPC21268) [7].

Gene context of Opc 31260

To determine if CD cAMP, generated from increased AVP-V2Rs, was accelerating the PKD, cystic mice and their normal littermates were treated with OPC31260, a relatively specific AVP-V2R antagonist [1].
V2R mRNA expression in kidney was significantly less in Tg rats than in control rats under basal conditions, and this suppression was restored by OPC31260 treatment to levels comparable with those of control rats [2].

Analytical, diagnostic and therapeutic context of Opc 31260

These results indicate that OPC31260 may be an effective treatment for these disorders and that clinical trials should be considered [5].

References

Developmental expression of urine concentration-associated genes and their altered expression in murine infantile-type polycystic kidney disease. Gattone, V.H., Maser, R.L., Tian, C., Rosenberg, J.M., Branden, M.G. Dev. Genet. (1999) [Pubmed]
Adaptation to sustained high plasma vasopressin in water and electrolyte homeostasis in the rat transgenic for the metallothionein-vasopressin fusion gene. Yokoi, H., Nagasaki, H., Tachikawa, K., Arima, H., Murase, T., Miura, Y., Hirabayashi, M., Oiso, Y. J. Endocrinol. (2002) [Pubmed]
Regulation of aquaporin mRNA expression in rat kidney by water intake. Murillo-Carretero, M.I., Ilundáin, A.A., Echevarria, M. J. Am. Soc. Nephrol. (1999) [Pubmed]
Effective treatment of an orthologous model of autosomal dominant polycystic kidney disease. Torres, V.E., Wang, X., Qian, Q., Somlo, S., Harris, P.C., Gattone, V.H. Nat. Med. (2004) [Pubmed]
Inhibition of renal cystic disease development and progression by a vasopressin V2 receptor antagonist. Gattone, V.H., Wang, X., Harris, P.C., Torres, V.E. Nat. Med. (2003) [Pubmed]
Vasodilation induced by vasopressin V2 receptor stimulation in afferent arterioles. Tamaki, T., Kiyomoto, K., He, H., Tomohiro, A., Nishiyama, A., Aki, Y., Kimura, S., Abe, Y. Kidney Int. (1996) [Pubmed]
Secretion of adrenomedullin by renal tubular cell lines. Sato, K., Imai, T., Iwashina, M., Marumo, F., Hirata, Y. Nephron (1998) [Pubmed]

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