GSK484 hydrochloride | PAD4 inhibitor

GSK484 chemical structure

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GSK484 (1652591-81-5) is a potent (IC50 = 50 nM) and selective inhibitor of protein arginine deiminase (PAD4).1 It blocks neutrophil extracellular trap formation in human neutrophils.1,2 GSK484 abrogates thrombus formation on heparin-induced thrombocytopenia/thrombosis.3 It protected against reperfusion injury in both stroke4 and cardiac5 models.  GSK484 attenuated tumor cell stemness in esophageal squamous cell carcinoma.6 It prevented surgery-induced tumor recurrence via inhibition of neutrophil extracellular trap-induced reprogramming of cancer cell metabolism.7

References/Citations:

  1. Lewis et al. (2015), Inhibition of PAD4 activity is sufficient to disrupt mouse and human NET formation; Nat. Chem. Biol., 11 189
  2. Clark et al. (2018), Protein Deiminase 4 and CR3 Regulate Aspergillus fumigatus and ß-Glucan-Induced Neutrophil Extracellular Trap Formation, but Hyphal Killing is Dependent Only on CR3; Front. Immunol., 9 1182
  3. Perdomo et al. (2019), Neutrophil activation and NETosis are the major drivers of thrombosis in heparin-induced thrombocytopenia; Nat. Commun., 10 1322
  4. Chen et al. (2025), Neutrophil Extracellular Traps Promote AIM2-Dependent Microglial Pyroptosis Following Stroke; Aging Dis., 17 3
  5. Mand et al. (2025), Peptidylarginine deiminase 4 deficiency alleviates hypoxia/reoxygenation-induced cardiomyocyte injury; PLoS One, 20 e0330864
  6. Wang et al. (2025), PADI4 facilitates stem-like properties and cisplatin resistance through upregulating PRMT2/IDs family in oesophageal squamous cell carcinoma; Clin.Transl. Med., 15 e70272
  7. Haykal et al. (2025), Surgery-Induced Neutrophil Extracellular Traps Promote Tumor Metastasis by Reprogramming Cancer Cell Lipid Metabolism; Cancer Res., Preprint before publication
1652591-81-5, 1652629-23-6, GSK 484, GSK484, GSK484 HCl, GSK484 supplier, NETosis inhibitor, PAD4 inhibitor

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GSK484 (1652591-81-5) is a potent (IC50 = 50 nM) and selective inhibitor of protein arginine deiminase (PAD4).1 It blocks neutrophil extracellular trap formation in human neutrophils.1,2 GSK484 abrogates thrombus formation on heparin-induced thrombocytopenia/thrombosis.3 It protected against reperfusion injury in both stroke4 and cardiac5 models.  GSK484 attenuated tumor cell stemness in esophageal squamous cell carcinoma.6 It prevented surgery-induced tumor recurrence via inhibition of neutrophil extracellular trap-induced reprogramming of cancer cell metabolism.7

References/Citations:

  1. Lewis et al. (2015), Inhibition of PAD4 activity is sufficient to disrupt mouse and human NET formation; Nat. Chem. Biol., 11 189
  2. Clark et al. (2018), Protein Deiminase 4 and CR3 Regulate Aspergillus fumigatus and ß-Glucan-Induced Neutrophil Extracellular Trap Formation, but Hyphal Killing is Dependent Only on CR3; Front. Immunol., 9 1182
  3. Perdomo et al. (2019), Neutrophil activation and NETosis are the major drivers of thrombosis in heparin-induced thrombocytopenia; Nat. Commun., 10 1322
  4. Chen et al. (2025), Neutrophil Extracellular Traps Promote AIM2-Dependent Microglial Pyroptosis Following Stroke; Aging Dis., 17 3
  5. Mand et al. (2025), Peptidylarginine deiminase 4 deficiency alleviates hypoxia/reoxygenation-induced cardiomyocyte injury; PLoS One, 20 e0330864
  6. Wang et al. (2025), PADI4 facilitates stem-like properties and cisplatin resistance through upregulating PRMT2/IDs family in oesophageal squamous cell carcinoma; Clin.Transl. Med., 15 e70272
  7. Haykal et al. (2025), Surgery-Induced Neutrophil Extracellular Traps Promote Tumor Metastasis by Reprogramming Cancer Cell Lipid Metabolism; Cancer Res., Preprint before publication