For research use only. Not for therapeutic Use.
ML141（Cat No.:I004661）is a selective inhibitor of Cdc42, a small GTPase involved in regulating various cellular processes, including cytoskeleton organization, cell migration, and cell division. By inhibiting Cdc42, ML141 disrupts key signaling pathways associated with cancer cell proliferation and metastasis, making it a valuable tool for cancer research. It has shown promise in studies focused on tumor cell motility and invasion. Additionally, ML141 is used to investigate the role of Cdc42 in other biological processes such as immune cell function and neurodevelopment, offering insights into potential therapeutic applications.
| Catalog Number | I004661 |
| CAS Number | 71203-35-5 |
| Synonyms | 4-(5-(4-methoxyphenyl)-3-phenyl-4,5-dihydro-1H-pyrazol-1-yl)benzenesulfonamide |
| Molecular Formula | C22H21N3O3S |
| Purity | ≥95% |
| Target | Cdc42 |
| Solubility | DMSO: ≥ 55 mg/mL |
| Storage | 2-8°C |
| IC50 | 200 nM |
| IUPAC Name | 4-[3-(4-methoxyphenyl)-5-phenyl-3,4-dihydropyrazol-2-yl]benzenesulfonamide |
| InChI | InChI=1S/C22H21N3O3S/c1-28-19-11-7-17(8-12-19)22-15-21(16-5-3-2-4-6-16)24-25(22)18-9-13-20(14-10-18)29(23,26)27/h2-14,22H,15H2,1H3,(H2,23,26,27) |
| InChIKey | QBNZBMVRFYREHK-UHFFFAOYSA-N |
| SMILES | COC1=CC=C(C=C1)C2CC(=NN2C3=CC=C(C=C3)S(=O)(=O)N)C4=CC=CC=C4 |
| Reference | 1:Int J Hematol. 2015 Jan;101(1):5-12. doi: 10.1007/s12185-014-1690-z. Epub 2014 Oct 15. Cdc42 inhibitor ML141 enhances G-CSF-induced hematopoietic stem and progenitor cell mobilization.Chen C,Song X,Ma S,Wang X,Xu J,Zhang H,Wu Q,Zhao K,Cao J,Qiao J,Sun X,Li D,Zeng L,Li Z,Xu K, PMID: 25315193 DOI: 10.1007/s12185-014-1690-z </br><span>Abstract:</span> G-CSF is the most often used agent in clinical hematopoietic stem and progenitor cell (HSPC) mobilization. However, in about 10 % of patients, G-CSF does not efficiently mobilize HSPC in clinically sufficient amounts. Cdc42 activity is involved in HSPC mobilization. In the present study, we explore the impact of Cdc42 inhibitor ML141 on G-CSF-mediated HSPC mobilization in mice. We found that the use of ML141 alone only triggered modest HSPC mobilization effect in mice. However, combination of G-CSF and ML141 significantly promoted HPSC counts and colony forming units in peripheral blood, as compared to mice treated with G-CSF alone. ML141 did not significantly alter the levels of SDF-1 and MMP-9 in the bone marrow, when used alone or in combination with G-CSF. We also found that G-CSF administration significantly increases the level of GTP-bound Cdc42, but does not alter the expression of Cdc42 in the bone marrow. Our data indicate that the Cdc42 signal is a negative regulator in G-CSF-mediated HSPC mobilization, and that inhibition of the Cdc42 signal efficiently improves mobilization efficiency. These findings may provide a new strategy for efficient HSPC mobilization, especially in patients with poor G-CSF response. |
