1. GPCR/G Protein
    Neuronal Signaling
  2. GPR55
  3. CID 16020046

CID 16020046 

Cat. No.: HY-16697 Purity: 99.92%
Handling Instructions

CID 16020046 is a potent and selective GPR55 antagonist and inhibits GPR55 constitutive activity with an IC50 of 0.15 μM. CID 16020046 inhibits GPR55-mediated Ca2+ signaling and GPR55-mediated ERK1/2 phosphorylation. CID 16020046 reduces wound healing in endothelial cells and is involved in the regulation of platelet function.

For research use only. We do not sell to patients.

CID 16020046 Chemical Structure

CID 16020046 Chemical Structure

CAS No. : 834903-43-4

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Free Sample (0.5-1 mg)   Apply Now  
10 mM * 1 mL in DMSO USD 196 In-stock
Estimated Time of Arrival: December 31
10 mg USD 178 In-stock
Estimated Time of Arrival: December 31
50 mg USD 748 In-stock
Estimated Time of Arrival: December 31
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Based on 1 publication(s) in Google Scholar

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Description

CID 16020046 is a potent and selective GPR55 antagonist and inhibits GPR55 constitutive activity with an IC50 of 0.15 μM. CID 16020046 inhibits GPR55-mediated Ca2+ signaling and GPR55-mediated ERK1/2 phosphorylation. CID 16020046 reduces wound healing in endothelial cells and is involved in the regulation of platelet function[1].

In Vitro

CID 16020046 has weak activities close for inhibition of the acetylcholinesterase (pIC50=4.4), antagonism of the m-opioid receptor (pIC50=4.6), and blockade of KCNH2, the hERG channel (pIC50=4.6) 6 in human embryonic kidney (HEK)-G protein–coupled receptor 55 (GPR55) cells[1].
CID 16020046 (2.5 μM; for ≥25 minutes) significantly inhibits the lysophosphatidylinositol (LPI; 2.5 μM) induced ERK1/2 phosphorylation. CID 16020046 alone fails to induce intracellular Ca2+ release in HEK-GPR55, HEKCB1 cells and shows no ERK1/2 phosphorylation[1].
Pretreatment with CID16020046 (0.01, 0.1, 1, 10 μM) leads to a concentration-dependent decrease in GPR55-mediated NFAT activation, NF-kB activation, and SRE induction in response to 1 μM LPI or GSK319197A in HEKGPR55 and HEK-CB1 cells[1].
CID16020046 (2.5 μM) antagonizes GPR55-mediated activation and nuclear translocation of transcription factors but has no effect on CB1-mediated CREB activation[1].
Pretreatment CID16020046 (1 μM) abolished the LPI-induced stimulation of wound healing in HMVEC-Ls[1].

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

Western Blot Analysis

Cell Line: HEK-CB1 and HEK-CB2 cells[1]
Concentration: 2.5 μM
Incubation Time: For ≥25 minutes
Result: Significantly inhibited the LPI (2.5 μM) induced ERK1/2 phosphorylation.
Treatment alone showed no ERK1/2 phosphorylation and did not alter WIN55,212-2 (2.5 μM) induced ERK1/2 phosphorylation in HEK-CB1 and HEK-CB2 cells.
Molecular Weight

425.44

Formula

C₂₅H₁₉N₃O₄

CAS No.
SMILES

O=C(O)C1=CC=C(N(C2C3=CC=CC(O)=C3)C(C4=C2C(C5=CC=C(C)C=C5)=NN4)=O)C=C1

Shipping

Room temperature in continental US; may vary elsewhere.

Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
Solvent & Solubility
In Vitro: 

DMSO : 100 mg/mL (235.05 mM; Need ultrasonic)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 2.3505 mL 11.7525 mL 23.5051 mL
5 mM 0.4701 mL 2.3505 mL 4.7010 mL
10 mM 0.2351 mL 1.1753 mL 2.3505 mL
*Please refer to the solubility information to select the appropriate solvent.
In Vivo:
  • 1.

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.5 mg/mL (5.88 mM); Clear solution

  • 2.

    Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in saline)

    Solubility: ≥ 2.5 mg/mL (5.88 mM); Clear solution

  • 3.

    Add each solvent one by one:  10% DMSO    90% corn oil

    Solubility: ≥ 2.5 mg/mL (5.88 mM); Clear solution

*All of the co-solvents are provided by MCE.
References

Purity: 99.92%

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Keywords:

CID 16020046CID16020046CID-16020046GPR55G protein-coupled receptor 55Ca2+ERK1/2phosphorylationwoundhealingendothelialcellsplateletfunctionacetylcholinesterasem-opioidKCNH2 hERGHEKlysophosphatidylinositolLPIHMVECInhibitorinhibitorinhibit

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