(S)-(+)-Ibuprofen, the S(+)-enantiomer of ibuprofen, is an effective inhibitor of both COX-1 and COX-2 enzymes, with IC50 values of 2.1 μM and 1.6 μM, respectively. It is recognized for its analgesic, anti-inflammatory, anticancer, and antipyretic properties[1][2].
体内研究
In vivo, (S)-(+)-Ibuprofen administered at a dose of 15 mg/kg/day via intraperitoneal injection, five days a week for four weeks, significantly inhibits tumor growth in HCA-7 and HCT-15 xenografts in a nude mice model. This highlights its potential efficacy in anticancer therapies in clinical settings[2].
体外研究
In vitro studies have shown that (S)-(+)-Ibuprofen treatment at concentrations ranging from 0 to 1000 µM over 8 days reduces cell survival in a concentration-dependent manner in both HCT-15 and HCA-7 cancer cell lines[2].
Additionally, treatment with (S)-(+)-Ibuprofen in these cell lines over 20 to 72 hours induces a block in the G0/G1 phase of the cell cycle and promotes apoptosis, demonstrating its potential to hinder cell cycle progression and trigger cancer cell death[2].
Further investigation into the cellular mechanisms of (S)-(+)-Ibuprofen revealed that at 900 µM for 4 to 72 hours, it downregulates cyclin A and B and increases the expression of the cell cycle inhibitory protein p27Kip-1, further substantiating its role in cell cycle regulation[2].
(S)-(+)-Ibuprofen's action extends beyond the cancer cell inhibition, as it also reduces COX activity, thromboxane production, and platelet aggregation, contributing to its broad pharmacological effects[1].
Ibuprofen also effectively inhibits the activation of the transcription factor NF-κB in response to T-cell stimulation, with an IC50 of 61.7 μM, which plays a significant role in inflammatory responses[3].
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