Catalog No.S8141

Cl-amidine Chemical Structure

Molecular Weight(MW): 424.8

Cl-amidine is an irreversible pan-peptidylarginine deiminase (PAD) inhibitor with IC50 values of 5.9 ± 0.3 μM, 0.8 ± 0.3 μM, 6.2 ± 1.0 μM for PAD4, PAD1 and PAD3, respectively.

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Description Cl-amidine is an irreversible pan-peptidylarginine deiminase (PAD) inhibitor with IC50 values of 5.9 ± 0.3 μM, 0.8 ± 0.3 μM, 6.2 ± 1.0 μM for PAD4, PAD1 and PAD3, respectively.
PAD1 [1]
(Cell-free assay)
PAD4 [1]
(Cell-free assay)
PAD3 [1]
(Cell-free assay)
0.8 μM 5.9 μM 6.2 μM
In vitro

Cl-amidine antagonizes the PAD4-mediated enhancement of the the p300GBD-GRIP1 interaction in a dose-dependent manner. The inhibitory effect of this compound is not a nonspecific one but is targeted at the active PAD4 enzyme[1]. Cl-amidine increases p53 expression in CD45 positive immune cells. It triggers the differentiation and apoptosis of multiple cancer cell lines that are p53+/+ and p53−/− (e.g., HL60, HT29, TK6, and U2-OS cells). Cl-amidine induces the expression of p53 and several downstream target genes including the cyclin dependent kinase inhibitor p21, GADD45, and the proapoptotic protein PUMA in U2-OS osteosarcoma cells[2].

In vivo Cl-amidine treatment inhibits NZM(New Zealand mixed 2328) NET(neutrophil extracellular trap) formation in vivo and significantly alters circulating autoantibody profiles and complement levels while reducing glomerular IgG deposition. Further, Cl-amidine increases the differentiation capacity of bone marrow endothelial progenitor cells, improves endothelium-dependent vasorelaxation, and markedly delays time to arterial thrombosis induced by photochemical injury. Cl-amidine delays thrombosis development in NZM mice. It inhibits PADs in mice without significant toxicity and improves disease phenotypes in animal models of inflammatory arthritis and inflammatory bowel disease[3]. And It is shown to reduce disease severity in mouse models of ulcerative colitis and RA[2].


Cell Research:


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  • Cell lines: CV-1 cells
  • Concentrations: 0-200 μM
  • Incubation Time: 40 h
  • Method:

    CV-1 cells are transiently transfected with plasmids encoding a luciferase reporter construct, p300GBD fused to the Gal4 DNA binding domain, the p300 binding domain of GRIP1 (i.e., the AD1 domain) fused to the VP16 activation domain (AD), and either wild-type PAD4 or the catalytically defective C645S mutant. Cl-amidine (0-200 μM) is then added to the cell culture medium and incubated for 40 h. Cell extracts are then prepared, and the luciferase activity present in these extracts is quantified. 

    (Only for Reference)
Animal Research:


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  • Animal Models: DSS mouse model of colitis (genetic background:C57BL/6 mice)
  • Formulation: 1× PBS
  • Dosages: 75 mg/kg (i.p); 5, 25, and 75 mg/kg(oral)
  • Administration: by oral gavage or i.p
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 84 mg/mL warmed (197.74 mM)
Ethanol 84 mg/mL warmed (197.74 mM)
Water 70 mg/mL warmed (164.78 mM)

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 424.8


CAS No. 1043444-18-3
Storage powder
in solvent
Synonyms N/A

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID