Mps1-IN-1 dihydrochloride
Based on 5 publication(s) in Google Scholar
Mps1-IN-1 dihydrochloride is a potent and ATP-competitive Mps1 kinase inhibitor with an IC50 of 367 nM. Mps1-IN-1 dihydrochloride inhibit Mps1 mitotic kinase activity and abrogates spindle assembly checkpoint (SAC) function. Mps1-IN-1 dihydrochloride decreases the viability of both cancer and ‘normal’ cells.
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- CAS No.: 1883548-93-3
- Formula: C28H35Cl2N5O4S
- Molecular Weight:608.58
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) Mps1-IN-1 dihydrochloride
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Biological Activity
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Mps1 367 nM (IC50) |
Mps1 27 nM (Kd) |
ALK 21 nM (Kd) |
LTK 29 nM (Kd) |
PYK2 280 nM (Kd) |
FAK 440 nM (Kd) |
IGF1R 750 nM (Kd) |
INSR 470 μM (Kd) |
CLK1 1900 nM (Kd) |
ERK2 2900 nM (Kd) |
INSRR 1200 nM (Kd) |
TNK1 2600 nM (Kd) |
TNK2 3100 nM (Kd) |
GAK 1100 nM (Kd) |
Mps1-IN-1 dihydrochloride (2-10 μM; 96 hours) inhibits the proliferative capacity of HCT116 cells to 33% that of DMSO control[1].
Mps1-IN-1 dihydrochloride (0.3-10 μM; 4 hours) induces bypass of a checkpoint-mediated mitotic arrest in a dose-dependent manner. Mps1-IN-1 dihydrochloride (10 μM) administration results in a dose-dependent decrease in the time spent in mitosis with nearly 100% U2OS cells initiating anaphase within 20 minutes[1].
Mps1-IN-1 dihydrochloride (0.5, 2, 10 μM) causes a dose-dependent reduction in hyper-phosphorylated Mps1 as demonstrated by a decrease in phosphorylation-induced mobility shift in UTRM10 LAP-Mps1 WT cells[1].
Mps1-IN-1 (5, 10 μM) arrested in mitosis using Nocodazole, results in a dose-dependent accumulation of 4c pHistone H3 negative cells in U2OS cells[1].
Acceleration of mitosis kinetics in Mps1-IN-1-treated cells had direct consequences on genomic stability with cells exhibiting significant signs of chromosome mis-alignment and chromosome mis-segregation[1].
Mps1-IN-1 dihydrochloride demonstrates greater than 1000-fold selectivity relative to the 352 member kinase panel with the major exceptions of Alk and Ltk[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HCT116 cells
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Concentration:2, 5, 10 μM
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Incubation Time:96 hours
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Result:The proliferative capacity of HCT116 cells was reduced to 33% that of DMSO control.
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Cell Line:U2OS cells
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Concentration:0.3, 0.5, 1, 2, 5, 10 μM
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Incubation Time:4 hours
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Result:Dropped levels of cyclin B protein, which accumulate in G2 and are sustained during an activated spindle checkpoint.
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Cell Line:Hela and U2OS cells
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Concentration:10 μM
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Incubation Time:Pretreatment 1 hour before taxol and MG132
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Result:Caused a dose-dependent reduction in the phosphorylation status of Aurora B at threonine-232 (Thr232).
Chemical Information
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CAS No. 1883548-93-3
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Molecular Weight 608.58
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Formula C28H35Cl2N5O4S
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SMILES
OC1CCN(C2=CC=C(NC3=CC(NC4=CC=CC=C4S(=O)(C(C)C)=O)=C5C(NC=C5)=N3)C(OC)=C2)CC1.[H]Cl.[H]Cl
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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.
Publications (5)
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Journal Impact Factor
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Most Recent
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Nat Commun
Human iPSC-based Modeling of Pulmonary Fibrosis Reveals p300/CBP Inhibition Suppresses Alveolar Transitional Cell State. [Abstract]2026 Feb 12;17(1):1214. PMID: 41680175 -
J Cancer
Proline-rich acidic protein 1 upregulates mitotic arrest deficient 1 to promote cisplatin-resistance of colorectal carcinoma by restraining mitotic checkpoint complex assembly. [Abstract]2023 May 21;14(9):1515-1530. PMID: 37325046 -
J Cell Biochem
Mps1 controls spindle assembly, SAC, and DNA repair in the first cleavage of mouse early embryos. [Abstract]2021 Feb;122(2):290-300. PMID: 33025669 -
Mol Reprod Dev
Phospholipase D2 Regulates Microtubule Acetylation by Modulating Gsk3β-Tau Signaling in Mouse Oocytes During Meiotic Maturation. [Abstract]2025 Aug;92(8):e70051. PMID: 40838360 -
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)