Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial hyperplasia, joint inflammation, and progressive dysfunction. Among its mediators, nitric oxide (NO) plays a dual role: while essential for host defense, its excessive production contributes to cytotoxicity and tissue damage. Propionic acid derivatives, a major class of nonsteroidal anti-inflammatory drugs (NSAIDs), reduce inflammation partly through inhibition of inducible nitric oxide synthase (iNOS) expression. 3-(4-Hydroxyphenyl)propionic acid, a propionic acid derivative, has been suggested as a potential therapeutic candidate for RA. This study aimed to investigate the effects of 3-(4-Hydroxyphenyl) propionic acid on cell viability and NO production in phorbol myristate acetate (PMA)-induced and unstimulated synovial fibroblasts (HIG-82). HIG-82 cells were cultured to 85–100% confluence and treated with eight concentrations of 3-(4-Hydroxyphenyl)propionic acid (3.125–300 µM). Ibuprofen and diclofenac (100 µM) served as positive controls. Treatments were applied for 24, 48, and 72 hours. Cell viability was assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, while NO production was determined via the Griess reaction. Absorbance was measured using an enzyme-linked immunosorbent assay (ELISA) microplate reader. Data were analyzed with one-way Analysis of Variance (ANOVA) followed by Tukey’s test and two-way ANOVA followed by Bonferroni’s post hoc test using GraphPad Prism 5. MTT assays showed that 3-(4-Hydroxyphenyl) propionic acid was not cytotoxic to either PMA-induced or unstimulated HIG-82 cells across all tested concentrations (P > 0.05 vs. controls). Cell viability declined with longer incubation times. NO production was not significantly suppressed by 3-(4-Hydroxyphenyl)propionic acid, with only transient effects observed at 24 and 48 hours in unstimulated cells. In conclusion, 3-(4-Hydroxyphenyl)propionic acid, ibuprofen, and diclofenac demonstrated no cytotoxicity in HIG-82 synovial fibroblasts. However, unlike standard NSAIDs, 3-(4-Hydroxyphenyl)propionic acid did not effectively inhibit NO production, suggesting limited potential as an anti-inflammatory agent through iNOS modulation.