Crisdesalazine | PGE2 synthase inhibitor

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Crisdesalazine (927685-43-6) is a potent inhibitor of microsomal prostaglandin E2 synthase-1 (IC50 = 230 nM).1 It also acted as a potent spin-trapping molecule and completely removed free radical at 50 nM. Crisdesalazine displayed efficacy in mouse models of ALS1 and Alzheimer’s disease2. In a mouse model of spinal cord injury, it inhibited proliferation of astrocytes via hydrogen peroxide inhibition and promoted nerve regeneration.3 It also significantly alleviated clinical symptoms in a mouse model of multiple sclerosis by promoting the M1 to M2 phase transition in macrophages.4 Crisdesalazine in combination with cisplatin restored CD8+ T cell function and significantly improved efficacy compared to cisplatin monotherapy in an ovarian cancer model.5

References/Citations:

  1. Shin et al. (2012), Concurrent blockade of free radical and microsomal prostaglandin E synthase-1-mediated PGE2 production improves safety and efficacy in a mouse model of amyotrophic lateral sclerosis; J. Neurochem. 122 952
  2. Baek et al. (2013), AAD-2004 Attenuates Progressive Neuronal Loss in the Brain of Tg-betaCTF99/B6 Mouse Model of Alzheimer Disease; Exp. Neurobiol. 22 31
  3. Xiaodan et al. (2025), AAD-2004 through clearing of H2O2 reduces astrocyte proliferation and promotes neural regeneration after spinal cord injury; Sci. Rep. 16 3371
  4. Park et al. (2025), Crisdesalazine alleviates inflammation in an experimental autoimmune encephalomyelitis multiple sclerosis mouse model by regulating the immune system; BMC Neurosci. 26 1
  5. Wu et al. (2026), Dynamic changes of the immune microenvironment in ovarian cancer following neoadjuvant chemotherapy; Cell Death Discov. 12 130
927685-43-6. PGE2 synthase inhibitor, AAD-2004, AAD-2004 supplier, crisdesalazine, Crisdesalazine supplier, m-PGE2 synthase inhibitor, prostaglandin E2 synthase inhibitor
Alternate Name:
AAD-2004

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Crisdesalazine (927685-43-6) is a potent inhibitor of microsomal prostaglandin E2 synthase-1 (IC50 = 230 nM).1 It also acted as a potent spin-trapping molecule and completely removed free radical at 50 nM. Crisdesalazine displayed efficacy in mouse models of ALS1 and Alzheimer’s disease2. In a mouse model of spinal cord injury, it inhibited proliferation of astrocytes via hydrogen peroxide inhibition and promoted nerve regeneration.3 It also significantly alleviated clinical symptoms in a mouse model of multiple sclerosis by promoting the M1 to M2 phase transition in macrophages.4 Crisdesalazine in combination with cisplatin restored CD8+ T cell function and significantly improved efficacy compared to cisplatin monotherapy in an ovarian cancer model.5

References/Citations:

  1. Shin et al. (2012), Concurrent blockade of free radical and microsomal prostaglandin E synthase-1-mediated PGE2 production improves safety and efficacy in a mouse model of amyotrophic lateral sclerosis; J. Neurochem. 122 952
  2. Baek et al. (2013), AAD-2004 Attenuates Progressive Neuronal Loss in the Brain of Tg-betaCTF99/B6 Mouse Model of Alzheimer Disease; Exp. Neurobiol. 22 31
  3. Xiaodan et al. (2025), AAD-2004 through clearing of H2O2 reduces astrocyte proliferation and promotes neural regeneration after spinal cord injury; Sci. Rep. 16 3371
  4. Park et al. (2025), Crisdesalazine alleviates inflammation in an experimental autoimmune encephalomyelitis multiple sclerosis mouse model by regulating the immune system; BMC Neurosci. 26 1
  5. Wu et al. (2026), Dynamic changes of the immune microenvironment in ovarian cancer following neoadjuvant chemotherapy; Cell Death Discov. 12 130