2. GPCR/G Protein Cell Cycle/DNA Damage
  3. Prostaglandin Receptor PERK
  4. ONO-8130

ONO-8130 is an orally active and selective prostanoid EP1 receptor antagonist. ONO-8130 blocks phosphorylation of ERK in the L6 spinal cord. ONO-8130 relieves bladder pain in mice with cyclophosphamide-induced cystitis. ONO-8130 can be used for interstitial cystitis research.

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ONO-8130 Chemical Structure

ONO-8130 Chemical Structure

CAS No. : 459841-96-4

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Description

ONO-8130 is an orally active and selective prostanoid EP1 receptor antagonist. ONO-8130 blocks phosphorylation of ERK in the L6 spinal cord. ONO-8130 relieves bladder pain in mice with cyclophosphamide-induced cystitis. ONO-8130 can be used for interstitial cystitis research[1].

In Vivo

ONO-8130 (0.3-30 mg/kg; Oral preadministration, once) strongly prevents both the bladder pain-like behavior and referred hyperalgesia in a dose-dependent manner[1].
ONO-8130 (30 mg/kg; Orally, once) reverses the established cystitis-related bladder pain[1].
ONO-8130 (30 mg/kg; Orally, once) strongly inhibits phosphorylation of ERK in MDH, DCM, and SPN of the L6 spinal cord caused by intravesical administration of PGE2[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Female ddY mice (18-22 g, 4-5 weeks old)[1]
Dosage: 0.3, 3, 10, and 30 mg/kg
Administration: Orally, once
Result: Strongly prevented both the bladder pain-like behavior and referred hyperalgesia in a dose-dependent manner, but had slight effect on the increased bladder weight and vascular permeability.
Animal Model: Female ddY mice (18-22 g, 4-5 weeks old, established bladder pain caused by IP cyclophosphamide)[1]
Dosage: 10, 30 mg/kg
Administration: Orally, once (administered 2.75 hours after i.p. cyclophosphamide)
Result: Markedly attenuated the bladder pain-like nociceptive behavior and referred hyperalgesia in the acute phase (3.5-4 h after cyclophosphamide).
Animal Model: Female ddY mice (18-22 g, 4-5 weeks old, established bladder pain caused by IP cyclophosphamide)[1]
Dosage: 30 mg/kg
Administration: Orally, once (administered 4.75 hours after i.p. cyclophosphamide)
Result: Significantly suppressed the bladder pain-like nociceptive behavior and tended to reduce the referred hyperalgesia in the persistent phase, 5.5-6 hours after cyclophosphamide.
Animal Model: Female ddY mice (18-22 g, 4-5 weeks old, intravesical administration of PGE2 at 5 nmol/mouse)[1]
Dosage: 30 mg/kg
Administration: Orally, once
Result: Strongly inhibited phosphorylation of ERK in MDH, DCM, and SPN of the L6 spinal cord caused by intravesical administration of PGE2 at 5 nmol/mouse, exerted complete blockade in DCM, while its inhibitory effects in MDH and SPN were partial.
Molecular Weight

500.63

Formula

C25H28N2O5S2
CAS No.
SMILES

O=[S](N(C(C=C(CCC1)C1=C2)=C2OCC(C=C3)=CC=C3C(O)=O)CC(C)C)(C4=NC(C)=CS4)=O
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References
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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

ONO-8130459841-96-4ONO8130ONO 8130Prostaglandin ReceptorPERKProtein kinase R-like endoplasmic reticulum kinasePKR-like endoplasmic reticulum kinaseOrally activeInterstitial cystitisBladder painHyperalgesiaInhibitorinhibitorinhibit

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