[CAS NO. 877636-42-5] ML221

Name: ML221
Brand: Arctom Scientific
SKU: SLK-S8695

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PRODUCTS SPECIFICATIONS [877636-42-5]

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Catalog

SLK-S8695

Brand

Selleck

CAS

877636-42-5

DESCRIPTION [877636-42-5]

Overview

MDL	MFCD06407006
Molecular Weight	385.35
Molecular Formula	C17H11N3O6S
SMILES	O=C1C=C(CSC2=NC=CC=N2)OC=C1OC(C3=CC=C([N+]([O-])=O)C=C3)=O

For research use only.

Storage

3 years,-20°C,powder
1 years,-80°C,in solvent

Shipping

Room temperature shipping(Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Concentration Volume Mass	1 mg	5 mg	10 mg
1 mM	2.5950 mL	12.9752 mL	25.9504 mL
5 mM	0.5190 mL	2.5950 mL	5.1901 mL
10 mM	0.2595 mL	1.2975 mL	2.5950 mL
50 mM	-	-	-

Description

ML221 is a potent apelin receptor (APJ) functional antagonist in cell-based assays that is >37-fold selective over the closely related angiotensin II type 1 (AT1) receptor. The IC50 values of ML221 are 0.70 and 1.75 μM in a cAMP assay and β-arrestin assay, respectively.

Targets

apelin receptor ^[1]
(β-arrestin assay)

1.75 μM

In vitro

In a PAMPA permeability assay, ML221 exhibits moderate permeability. ML221 displays moderate plasma and poor microsomal stability, as it is rapidly metabolized in both human and mouse liver homogenates (4.2% and 4.9% remaining at 60 min). It shows no toxicity (>50 μM) toward human hepatocytes. ML221 displays limited cross reactivity against a range of GPCRs. ML221 inhibits endothelial cell proliferation by blocking apelin-APJ signaling without affecting the expression of VEGF and VEGFR2.

In vivo

Intraperitoneal administration of ML221 inhibits pathological angiogenesis but enhances the recovery of normal vessels into the ischemic regions in the retina of the OIR model mice. A single application of ML221 alleviates mechanical allodynia and heat hyperalgesia 7 days following chronic constriction injury (CCI), in a dose‑dependent manner. Intraspinal delivery of ML221, at the onset of and in fully‑established neuropathic pain, persistently attenuates CCI‑induced pain hypersensitivity, indicating that the apelin‑APJ system is involved in initiating and maintaining pain. Intrathecal ML221 downregulates phosphorylated extracellular signal‑related kinase (ERK) in the rat spinal cord dorsal horn, suggesting that the effect of apelin on neuropathic pain may be mediated via ERK signaling.