1. Epigenetics
  2. Protein Arginine Deiminase

Protein Arginine Deiminase

Protein arginine deiminase (PAD), is a group of calcium-dependent enzymes, which play crucial roles in citrullination, and can catalyze arginine residues into citrulline. his chemical reaction induces citrullinated proteins formation with altered structure and function, leading to numerous pathological diseases, including inflammation and autoimmune diseases. These pathologies established the PADs as therapeutic targets and multiple PAD inhibitors are known.

Humans encode five PADs, designated PADs 1-4 and PAD6. Of the five PAD isozymes (PAD1, 2, 3, 4 and 6), only four (PADs1-4) are catalytically active. PAD activity is tightly regulated by Ca2+ and PADs contain 4 (PAD1), 5 (PAD3, 4) or 6 (PAD2) Ca2+-binding sites. Dysregulated PAD activity, most notably PAD2 and PAD4, is associated with multiple inflammatory diseases (e.g., rheumatoid arthritis) as well as cancer, and PAD inhibitors, such as Cl-amidine and BB-Cl-amidine, show efficacy in multiple preclinical animal models of disease.

Protein Arginine Deiminase Related Products (14):

Cat. No. Product Name Effect Purity
  • HY-100514
    GSK484 hydrochloride Inhibitor
    GSK484 hydrochloride is a selective and reversible peptidylarginine deiminase 4 (PAD4) inhibitor. GSK484 hydrochloride demonstrates high affinity binding to PAD4 with IC50s of 50 nM in the absence of Calcium. In the presence of 2 mM Calcium, notably lower potency (250 nM) is observed.
  • HY-100574A
    Cl-amidine hydrochloride Inhibitor
    Cl-amidine hydrochloride is an orally active peptidylarginine deminase (PAD) inhibitor, with IC50 values of 0.8 μM, 6.2 μM and 5.9 μM for PAD1, PAD3, and PAD4, respectively. Cl-amidine hydrochloride induces apoptosis in cancer cells. Cl-amidine hydrochloride induces microRNA (miR)-16 (miRNA-16, microRNA-16) expression and causes cell cycle arrest. Cl-Amidine hydrochloride prevents histone 3 citrullination and neutrophil extracellular trap formation, and improves survival in a murine sepsis model[1][2][3][4][5].
  • HY-111347A
    BB-Cl-Amidine hydrochloride Inhibitor
    BB-Cl-Amidine hydrochloride is a peptidylarginine deminase (PAD) inhibitor[1].
  • HY-137655A
    BMS-P5 free base Inhibitor 99.94%
    BMS-P5 free base is a specific and orally active peptidylarginine deiminase 4 (PAD4) inhibitor. BMS-P5 free base blocks MM-induced NET formation and delays progression of MM in a syngeneic mouse model[1].
  • HY-111347
    BB-Cl-Amidine Inhibitor
    BB-Cl-Amidine is a peptidylarginine deminase (PAD) inhibitor.
  • HY-125099
    PAD2-IN-2 Inhibitor
    PAD2-IN-2 is a potent PAD2 inhibitor. PAD2-IN-2 enters the HEK293T/PAD2 cells with an EC50 of 5.9 μM. PAD2-IN-2 inhibits histone H3 citrullination with an EC50 of 2.1 μM in HEK293/PAD2 cells. PAD2-IN-2 can be used for the research of cancer[1].
  • HY-100574D
    D-Cl-amidine hydrochloride Inhibitor 99.40%
    D-Cl-amidine hydrochloride is a potent and highly selective PAD1 inhibitor. D-Cl-amidine is well-torelated with no significant toxicity[1].
  • HY-124586
    Streptonigrin Inhibitor
    Streptonigrin (Bruneomycin), a natural product produced by Streptomyces flocculus, possesses both anti-tumor and anti-bacterial activity. Streptonigrin acts as a pan-PAD inhibitor with IC50s of 48.3±34.2 µM, 26.1±0.3 µM, 0.43±0.03 µM, and 2.5±0.4 µM for PAD1, PAD2, PAD3, and PAD4, respectively[1].
  • HY-B1505
    Acefylline Activator 99.89%
    Acefylline (Theophyllineacetic acid), a xanthine derivative, is an adenosine receptor antagonist. Acefylline is a peptidylarginine deiminase (PAD) activator. Acefylline is also a bronchodilator, which inhibits rat lung cAMP phosphodiesterase isoenzymes[1][2].
  • HY-100574
    Cl-amidine Inhibitor
    Cl-amidine is an orally active peptidylarginine deminase (PAD) inhibitor, with IC50 values of 0.8 μM, 6.2 μM and 5.9 μM for PAD1, PAD3, and PAD4, respectively. Cl-amidine induces apoptosis in cancer cells. Cl-amidine induces microRNA (miR)-16 (miRNA-16, microRNA-16) expression and causes cell cycle arrest. Cl-Amidine prevents histone 3 citrullination and neutrophil extracellular trap formation, and improves survival in a murine sepsis model[1][2][3][4][5].
  • HY-100574C
    D-Cl-amidine Inhibitor
    D-Cl-amidine is a potent and highly selective PAD1 inhibitor. D-Cl-amidine is well-torelated with no significant toxicity[1].
  • HY-136557
    PAD2-IN-1 Inhibitor
    PAD2-IN-1, a benzimidazole-based derivative, is a potent and selective protein arginine deiminase 2 (PAD2) inhibitor. PAD2-IN-1 shows superior selectivity for PAD2 over PAD4 (95-fold) and PAD3 (79-fold)[1].
  • HY-100574B
    Cl-amidine TFA Inhibitor
    Cl-amidine TFA is an orally active peptidylarginine deminase (PAD) inhibitor, with IC50 values of 0.8 μM, 6.2 μM and 5.9 μM for PAD1, PAD3, and PAD4, respectively. Cl-amidine TFA induces apoptosis in cancer cells. Cl-amidine TFA induces microRNA (miR)-16 (miRNA-16, microRNA-16) expression and causes cell cycle arrest. Cl-Amidine TFA prevents histone 3 citrullination and neutrophil extracellular trap formation, and improves survival in a murine sepsis model[1][2][3][4][5].
  • HY-137655
    BMS-P5 Inhibitor
    BMS-P5 is a specific and orally active peptidylarginine deiminase 4 (PAD4) inhibitor. BMS-P5 blocks MM-induced NET formation and delays progression of MM in a syngeneic mouse model[1].