r-Citalopram oxalate

• CAS: 219861-53-7
• Catalog Number: ACM219861537
• Category: Main Products
• Molecular Weight: 414.43
• Molecular Formula: C₂₀H₂₁FN₂O·C₂H₂O₄
• Synonyms: S-citalopram Oxalate
• IUPAC Name: (1R)-1-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-3H-2-benzofuran-5-carbonitrile;oxalicacid
• SMILES: CN(C)CCCC1(C2=C(CO1)C=C(C=C2)C#N)C3=CC=C(C=C3)F.C(=O)(C(=O)O)O
• InChI Key: KTGRHKOEFSJQNS-VEIFNGETSA-N
• Boiling Point: 591.2ºC at 760 mmHg
• Melting Point: 153-155ºC
• Flash Point: 311.3ºC
• Appearance: White Solid
• Exact Mass: 414.15900

Case Study

Functional Insights into R-Citalopram Oxalate in Inflammation-Induced Depression Models

Dong C, et al. Pharmacology Biochemistry and Behavior, 2016, 144, 7-12.

R-Citalopram oxalate, the inactive enantiomer of escitalopram, has been explored for its functional role in inflammation-induced depression models, highlighting its pharmacological differentiation. Unlike its counterpart escitalopram, R-citalopram oxalate lacks significant anti-inflammatory or antidepressant efficacy in lipopolysaccharide (LPS)-induced models of depression. Experimental evidence demonstrates that R-citalopram oxalate at a dose of 10 mg/kg does not influence serum levels of pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) or the anti-inflammatory cytokine interleukin-10 (IL-10) following LPS administration. Additionally, it fails to mitigate behavioral despair, as observed in immobility time during tail-suspension and forced swimming tests.
These findings contrast starkly with the efficacy of escitalopram, which exhibits robust anti-inflammatory and antidepressant effects by modulating serotonergic pathways. The ineffectiveness of R-citalopram oxalate also extends to its co-administration with escitalopram, where it antagonizes the latter's therapeutic effects, suggesting potential interference with serotonergic activity.

R-Citalopram Oxalate: A Distinct Enantiomer with Reduced Electrophysiological Impact on Nav1.5 VGSCs

Nakatani Y, et al. European Journal of Pharmacology, 2021, 908, 174316.

R-Citalopram oxalate, the R-enantiomer of citalopram, demonstrates unique electrophysiological properties compared to its S-enantiomer, escitalopram. This distinction is critical in understanding its reduced cardiotoxic potential. In studies utilizing HEK293 cells expressing human Nav1.5 voltage-gated sodium channels (VGSCs), R-citalopram exhibited a significantly lower inhibitory effect on VGSC currents. At a concentration of 100 μM, R-citalopram decreased Nav1.5 VGSC currents by only 36.2 ± 8.7%, compared to 60.0 ± 6.3% for racemic citalopram and 55.1 ± 12.5% for escitalopram.
Furthermore, R-citalopram minimally altered the voltage-dependence of activation and inactivation of Nav1.5 VGSCs, unlike escitalopram, which induced a negative shift in these parameters. This suggests that the adverse cardiac effects commonly associated with citalopram, including QTc prolongation, are predominantly mediated by escitalopram.