MRS2693 ammonium
MRS2693 ammonium is a selective P2Y6 receptor agonist. MRS2693 ammonium exerts biological effects by activating the Gq-coupled P2Y6 receptor, the ERK1/2 pathway, and the P2RY6-PLCB3-CAMKK2-PRKAA1-ULK1 signaling cascade. MRS2693 ammonium attenuates TNFα-induced NF-κB activation, stabilizes XIAP via AKT-mediated phosphorylation, induces autophagy, and reactivates PRKAA1. MRS2693 ammonium can be used in research on diseases including skeletal muscle ischemia/reperfusion injury, TNFα-induced skeletal muscle apoptosis, chronic myelomonocytic leukemia, colorectal cancer, and dry eye disease.
For research use only. We do not sell to patients.
- CAS No.: 911391-37-2
- Formula: C9H22IN5O12P2
- Molecular Weight:581.15
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All P2Y Receptor Isoforms
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Biological Activity
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XIAP |
ERK1 |
ERK2 |
P2Y6 Receptor |
MRS2693 ammonium (10-30 μM; 4 h-4 days) restores autophagy and normal differentiation of primary CD14+CD24- monocytes from a CMML patient co-cultured with CD14-CD24+ immature granulocytes, via reactivation of PRKAA1, while 10 μM MRS2693 ammonium partially increases PRKAA1 expression[2].
MRS2693 ammonium (1.5 μM; 15 min pre-incubation; continued during 4 h TNFα/CHX treatment and subsequent 16 h incubation) protects HT-29 colon carcinoma cells from TNFα-induced apoptosis by stabilizing XIAP via AKT-mediated phosphorylation, resulting in reduced PARP cleavage[3].
MRS2693 ammonium (1.5 μM; 30 min pre-incubation; continued during 24 h 5-FU treatment) induces resistance to 5-FU cytotoxicity in mouse CRC-derived tumoroids, preserving both tumoroid viability and proliferative cell activity[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:mouse skeletal C2C12 myoblasts/myotubes
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Concentration:0.1-100 nM (apoptosis assay); 10 nM (PKC expression analysis; ERK1/2 activation analysis; NF-κB attenuation analysis)
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Incubation Time:4 h (apoptosis assay, prior to medium change, total 20 h post-TNFα exposure); 20 min (PKC expression analysis); null (ERK1/2 activation analysis); null (NF-κB attenuation analysis)
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Result:Protected C2C12 cells against TNFα-induced apoptosis in a concentration-dependent manner between 0.1 and 10 nM, with protection diminished at 100 nM.
Provided 50-60% protection against TNFα-induced cell death in 5 and 7 day old C2C12 cultures at 10 nM and 100 nM.
Increased phosphorylated ERK1/2 levels by 3.4-fold at 10 nM.
Increased PKCθ expression after 20 min at 10 nM.
Attenuated the marked increase in NF-κB expression induced by 4 h TNFα exposure at 10 nM.
Showed no effect on cell death in the absence of TNFα, and only slightly increased NF-κB levels when used alone.
Had protective effects completely blocked by pre-incubating cells with 10 μM MRS2578 for 20 min at 10 nM.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL6 (2.5- to 3-months-old, weighing ~25 g, skeletal muscle injury induced by 90 minutes of hindlimb ischemia followed by 24 hours of reperfusion)[1]
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Dosage:1 mg/kg
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Administration:i.p.; single injection 2 hours before ischemia induction
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Result:Reduced serum creatine kinase (CK) activity to 3450 U/L.
Reduced the percentage of Evans Blue dye (EBD)-stained injured muscle area to 10.4%.
Lowered serum CK activity by ~72.6% compared to vehicle-treated controls.
Lowered EBD-stained injured muscle area by ~63.2% compared to vehicle-treated controls.
Chemical Information
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CAS No. 911391-37-2
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Molecular Weight 581.15
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Formula C9H22IN5O12P2
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SMILES
O[C@H]1[C@@H](O)[C@H](N2C(NC(C(I)=C2)=O)=O)O[C@@H]1COP(O)(OP(O)(O)=O)=O.N.N.N
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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.
Purity & Documentation
References
[1]. Mamedova LK, et al. Attenuation of apoptosis in vitro and ischemia/reperfusion injury in vivo in mouse skeletal muscle by P2Y6 receptor activation. Pharmacological research. 2008;58(3-4):232-9. [Content Brief]
[2]. Obba S, et al. The PRKAA1/AMPKα1 pathway triggers autophagy during CSF1-induced human monocyte differentiation and is a potential target in CMML. Autophagy. 2015;11(7):1114-29. [Content Brief]
[4]. Fjærvoll KA, et al. Pyrimidinergic P2Y1-Like Nucleotide Receptors Are Functional in Rat Conjunctival Goblet Cells. Investigative ophthalmology & visual science. 2025 Jan 02;66(1):46. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)