ML141

• CAT Number: I004661
• CAS Number: 71203-35-5
• Molecular Formula: C22H21N3O3S
• Molecular Weight: 407.49
• Purity: ≥95%
• Synonyms: 4-(5-(4-methoxyphenyl)-3-phenyl-4,5-dihydro-1H-pyrazol-1-yl)benzenesulfonamide
• 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

ML141（Cat No.:I004661） is a highly potent and selective noncompetitive inhibitor of cdc42, a member of the Rho family of GTPases. It binds to cdc42 and reversibly inhibits its activity. With an IC50 (half-maximal inhibitory concentration) of 200 nM, ML141 effectively disrupts cdc42-mediated cellular functions. By specifically targeting cdc42, ML141 offers a valuable tool for studying the role of cdc42 in various biological processes and signaling pathways.

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 Abstract: 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.