Ingredients in Zyflamend, including holy basil, turmeric, ginger, green tea, rosemary, hu zhang, Chinese gold thread, and Scutellaria, inhibit COX-2 activity and thereby reduce inflammation.

In vitro, Zyflamend inhibited inflammatory enzymes, decreased retinoblastoma protein phosphorylation ⁽¹⁰⁾, and induced apoptosis in human prostate cancer cells ^{(2) (3) (4) (11)}. It also reduced androgen receptor signaling and enhanced bicalutamide-induced apoptosis ⁽⁹⁾. Other studies in prostate cancer cell lines suggest that Zyflamend inhibits class I and class II histone deacetylase expression, upregulates p21 expression ⁽¹³⁾, and regulates upstream kinases LKB1 and CaMKK2 via AMPK activation ⁽¹⁴⁾.

In melanoma cells, Zyflamend induced autophagy and apoptosis sequentially by activating the intrinsic caspase cascade. Cell migration and COX-2 expression were also suppressed ⁽⁵⁾. It also inhibited NF-kappa B activation in myeloid leukemia, lung adenocarcinoma ⁽²⁾, pancreatic ⁽⁴⁾, and cisplatin-resistant bladder cancer cells ⁽¹⁵⁾. In leukoplakia and skin cell lines, both Zyflamend and carnosol, an antioxidant phenolic constituent, inhibited mutagenesis via Hsp90 ATPase inhibition, which led to reduced aryl hydrocarbon receptor levels and CYP1A1 and CYP1B1 suppression ⁽¹²⁾.

Both a cellular model of obesity-related inflammation and an obese animal model indicate that Zyflamend blocks proinflammatory mediators and aromatase induction as well as Akt and NF-kB activation. Increased aromatase mRNA levels and mammary gland activity were also partially inhibited ⁽⁷⁾. Reduction of adiposity was attributed to AMPK activation ⁽¹⁶⁾.

In a murine xenograft model of prostate cancer, Zyflamend inhibited androgen-dependent tumor growth and histone deacetylase-5, biomarkers linked to prostate cancer progression ⁽⁶⁾. It also reduced the number of inflammatory cells, hyperplasia and dysplasia, and tumor incidence and number, and inhibited cell proliferation in an animal model of oral squamous cell carcinoma ⁽³⁾.