JMV 3008
JMV 3008 is a GHS-R1a antagonist with an IC50 of 5.6 nM. JMV 3008 can be used in the research of diseases such as diabetes and obesity.
For research use only. We do not sell to patients.
- CAS No.: 925239-09-4
- Formula: C36H39N7O3
- Molecular Weight:617.74
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
GHSR1a 5.6 nM (IC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HEK293 | IC50 |
5.6 nM
Compound: 2, JMV 3008
|
Antagonist activity at mouse GSH-R1a receptor expressed in HEK293 cells assessed as inhibition of ghrelin-induced calcium mobilization after 5 mins by FLIPR assay
Antagonist activity at mouse GSH-R1a receptor expressed in HEK293 cells assessed as inhibition of ghrelin-induced calcium mobilization after 5 mins by FLIPR assay
|
[PMID: 22342626] |
| LLC-PK1 | IC50 |
5.6 nM
Compound: JMV 3008
|
Displacement of 125I]-His9-ghrelin from human GHSR1a expressed in LLCPK1 cells
Displacement of 125I]-His9-ghrelin from human GHSR1a expressed in LLCPK1 cells
|
[PMID: 18193826] |
Chemical Information
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CAS No. 925239-09-4
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Molecular Weight 617.74
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Formula C36H39N7O3
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SMILES
O=C([C@H]1NCCC1)N[C@@H](C2=NN=C(CCC3=CNC4=C3C=CC=C4)N2CC5=CC=C(OC)C=C5OC)CC6=CNC7=C6C=CC=C7
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)