2. GPCR/G Protein Immunology/Inflammation NF-κB Metabolic Enzyme/Protease Apoptosis
  3. Prostaglandin Receptor PGE synthase Reactive Oxygen Species (ROS) Apoptosis
  4. Crisdesalazine

Crisdesalazine (AAD-2004) is a microsomal prostaglandin E2 synthase-1 (mPGES-1) inhibitor. Crisdesalazine acts as a potent free radical scavenger that directly neutralizes reactive oxygen species (ROS) including hydrogen peroxide, exerting neuroprotective effects against apoptosis and axonal damage. Crisdesalazine inhibits PGE2 production, mediates inflammatory responses, and promotes the conversion of macrophages from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype. Crisdesalazine is applicable to neuroprotection research in multiple sclerosis and spinal cord injury.

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Crisdesalazine

Crisdesalazine Chemical Structure

CAS No. : 927685-43-6

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Based on 1 publication(s) in Google Scholar

Crisdesalazine Related Antibodies

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Description

Crisdesalazine (AAD-2004) is a microsomal prostaglandin E2 synthase-1 (mPGES-1) inhibitor. Crisdesalazine acts as a potent free radical scavenger that directly neutralizes reactive oxygen species (ROS) including hydrogen peroxide, exerting neuroprotective effects against apoptosis and axonal damage. Crisdesalazine inhibits PGE2 production, mediates inflammatory responses, and promotes the conversion of macrophages from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype. Crisdesalazine is applicable to neuroprotection research in multiple sclerosis and spinal cord injury[1][2].

In Vitro

Crisdesalazine (0.2-50 μM; 24 h) is non-cytotoxic to murine RAW 264.7 macrophages at concentrations up to 50 μM and to human SH-SY5Y neuroblastoma cells at concentrations up to 10 μM, with reduced viability only at 50 μM in SH-SY5Y cells[1].
Crisdesalazine (0.2-5 μM; 24 h post-LPS stimulation) promotes the transition of LPS-stimulated murine RAW 264.7 macrophages from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype by reducing pro-inflammatory marker and cytokine expression and increasing anti-inflammatory marker expression[1].
Crisdesalazine (0.2-5 μM; 24 h during co-culture) reduces neuroinflammation and neuronal necrosis in human SH-SY5Y cells co-cultured with LPS-stimulated murine RAW 264.7 macrophages by suppressing pro-inflammatory cytokine expression and decreasing necrotic cell populations[1].
Crisdesalazine (1 mM) reduces H2O2 levels in primary mouse spinal cord astrocytes, attenuates astrocytic reactivity, and exerts neuroprotective effects against apoptosis and axonal injury in primary mouse cortical neurons co-cultured with OGD/R-challenged astrocytes[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Crisdesalazine Related Antibodies

Cell Viability Assay[1]

Cell Line: human neuroblastoma SH-SY5Y cells, murine macrophage RAW 264.7 cells
Concentration: 0.2, 1, 5, 10, 50 μM
Incubation Time: 24 h
Result: Significantly reduced SH-SY5Y cell viability only at the 50 μM concentration.
Did not affect RAW 264.7 cell viability at any tested concentration.

Real Time qPCR[1]

Cell Line: LPS-stimulated murine RAW 264.7 macrophages
Concentration: 0.2, 1, 5 μM; 10 μM (excluded from subsequent experiments)
Incubation Time: 24 h post-LPS stimulation
Result: Significantly reduced mRNA expression of M1 pro-inflammatory marker iNOS and pro-inflammatory cytokines IL-1β and IL-6 compared to LPS-stimulated untreated cells at 0.2, 1, and 5 μM.
Showed no significant effect on IL-6 expression at 10 μM.
Significantly increased CD206 (M2 anti-inflammatory marker) expression in treated groups compared to LPS-stimulated untreated groups via immunofluorescence staining.

Real Time qPCR[1]

Cell Line: co-culture system of LPS-stimulated murine RAW 264.7 macrophages and human neuroblastoma SH-SY5Y cells
Concentration: 0.2, 1, 5 μM
Incubation Time: 24 h during co-culture
Result: Significantly reduced mRNA expression of pro-inflammatory cytokines IL-1β, IL-6, and TNF-α in SH-SY5Y cells co-cultured with LPS-stimulated RAW 264.7 cells, with marked reductions seen at 0.2 and 5 μM.
Significantly reduced neuronal necrosis in all treated groups compared to untreated co-culture groups, with the greatest reduction observed at 0.2 μM.
In Vivo

Crisdesalazine (3.3 mg/kg; i.p.; daily; 7 days) significantly alleviates clinical symptoms, reduces inflammatory cell infiltration and demyelination, shifts microglia/macrophage polarization toward an anti-inflammatory M2 phenotype, and expands Treg populations in a mouse EAE model of multiple sclerosis[1].
Crisdesalazine (3.3 mg/kg; i.p.; daily; 14 days) reduces spinal cord H2O2 levels, inhibits glial scar formation and astrocyte proliferation, promotes neuronal and axonal regeneration, and improves motor function in a mouse model of spinal cord injury[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6 (6-week-old female; EAE induced by MOG35-55 immunization with complete Freund’s adjuvant plus pertussis toxin)[1]
Dosage: 3.3 mg/kg
Administration: i.p.; once daily; 7 days
Result: Significantly reduced EAE clinical symptom severity from day 11 to day 23 post-induction.
Decreased mononuclear cell infiltration and demyelination in the spinal cord.
Increased spinal cord expression of M2 anti-inflammatory marker CD206 and regulatory T cell marker Foxp3.
Decreased spinal cord expression of M1 pro-inflammatory marker iNOS and pro-inflammatory cytokines TNF-α, IFN-γ, IL-1β, and IL-6.
Increased percentage of CD4+CD25+Foxp3+ Treg cells in splenocytes.
Increased CD206 expression in splenocytes.
Decreased iNOS, TNF-α, and IFN-γ expression in splenocytes.
Reduced IL-6 secretion in splenocytes to levels similar to naïve mice.
Caused no drug-related adverse effects.
Animal Model: C57BL/6J (6-8 weeks old, 19-20 g, SPF grade, spinal cord injury induced via weight-drop contusion at T10 level)[2]
Dosage: 3.3 mg/kg
Administration: i.p.; daily; 14 days
Result: Significantly reduced spinal cord H2O2 concentration compared to vehicle-treated SCI mice.
Significantly improved BMS scores and hindlimb stride length at 21 days post-injury compared to vehicle-treated SCI mice.
Mitigated SCI-induced reduction in motor neuron number and preserved spinal cord tissue structure, with smaller lesion cavities compared to vehicle-treated SCI mice.
Significantly downregulated mean fluorescence intensity of GFAP and vimentin (markers of glial scar formation) compared to vehicle-treated SCI mice.
Significantly downregulated vimentin protein expression measured via western blot compared to vehicle-treated SCI mice.
Significantly reduced mean fluorescence intensity of Ki67+/GFAP+ and PH3+/GFAP+ (markers of astrocyte proliferation) compared to vehicle-treated SCI mice.
Significantly increased mean fluorescence intensity of Neun+ and MAP2+ (markers of neuronal regeneration) compared to vehicle-treated SCI mice.
Significantly increased mean fluorescence intensity of GAP43+ and NF+ (markers of axonal regeneration) compared to vehicle-treated SCI mice.
Molecular Weight

325.28

Formula

C16H14F3NO3
CAS No.
Appearance

Solid

Color

White to off-white

SMILES

OC(C1=CC(NCCC2=CC=C(C(F)(F)F)C=C2)=CC=C1O)=O
Shipping

Room temperature in continental US; may vary elsewhere.
Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
Solvent & Solubility
In Vitro: 

DMSO : 50 mg/mL (153.71 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 3.0743 mL 15.3714 mL 30.7427 mL
5 mM 0.6149 mL 3.0743 mL 6.1485 mL
View the Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

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Purity & Documentation

Purity: 98.92%

SDS (394 KB)

COA (246 KB) HNMR (319 KB) LCMS (88 KB)

Handling Instructions (2659 KB)
References

Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Optional Solvent Concentration Solvent Mass 1 mg 5 mg 10 mg 25 mg
DMSO 1 mM 3.0743 mL 15.3714 mL 30.7427 mL 76.8569 mL
5 mM 0.6149 mL 3.0743 mL 6.1485 mL 15.3714 mL
10 mM 0.3074 mL 1.5371 mL 3.0743 mL 7.6857 mL
15 mM 0.2050 mL 1.0248 mL 2.0495 mL 5.1238 mL
20 mM 0.1537 mL 0.7686 mL 1.5371 mL 3.8428 mL
25 mM 0.1230 mL 0.6149 mL 1.2297 mL 3.0743 mL
30 mM 0.1025 mL 0.5124 mL 1.0248 mL 2.5619 mL
40 mM 0.0769 mL 0.3843 mL 0.7686 mL 1.9214 mL
50 mM 0.0615 mL 0.3074 mL 0.6149 mL 1.5371 mL
60 mM 0.0512 mL 0.2562 mL 0.5124 mL 1.2809 mL
80 mM 0.0384 mL 0.1921 mL 0.3843 mL 0.9607 mL
100 mM 0.0307 mL 0.1537 mL 0.3074 mL 0.7686 mL
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Crisdesalazine Related Classifications

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Crisdesalazine927685-43-6AAD-2004AAD2004AAD 2004Prostaglandin ReceptorPGE synthaseReactive Oxygen Species (ROS)ApoptosisProstaglandin E synthaseprimary cortical cellsM2hydrogen peroxidespinal cord demyelinationmicrosomal prostaglandin E2 synthase-1amyotrophic lateral sclerosis mouse modelsM1macrophageastrocyteprostaglandin E2Inhibitorinhibitorinhibit

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