The IC50, or inhibitory concentration necessary to block 50% DPPH free radicals, was used to quantify antioxidant activity using the DPPH technique. Several concentrations ranging from 25 to 200 µg/mL EECC were tested for antioxidant activity in the DPPH model. EECC showed a maximum antioxidant activity of 91.95% at 200 µg/mL with an IC50 value of 49.28 µg/mL.  
Tested samples showed a significant increase in antioxidant activity with increasing dosages. The DPPH technique employed ascorbic acid as a reference medication to measure antioxidant activity. At 200 µg/mL, the inhibition percentage was 98.05%, while the IC50 value was 20.88 µg/mL.  
This study's findings were summarized as the mean ± SEM for all four replicates with p<0.05 considered significant. In order to determine the IC50 value at 50% inhibition, we used the AAT Bioquest tool to analyze the regression graph.  
A dosage range of 500-5000 mg/kg for all test samples did not produce any mortality or unusual signs of toxicity or behavioral deviations during the acute oral toxicity test. The outcomes revealed that the research samples introduced in this study did not have toxic impacts on animal models up to 5000 mg/kg.  
At 200 mg/kg, the rectal temperature significantly decreased (p<0.05). The maximum antipyretic effect observed at a dose of 200 mg/kg was 90.50% (p<0.05), while those of 25, 50, and 100 mg/kg were 59.34%, 54.82%, and 71.87%, respectively. Paracetamol showed an estimated value of 97.29% (p<0.05).  
To keep the body temperature stable, the hypothalamus controls the body's temperature by balancing heat production and loss. Fever can be triggered by infections, tissue damage, or inflammation. Cytokines like interleukins and tumor necrosis factor-alpha migrate to the brain, activate the arachidonic acid pathway, and increase PGE2 synthesis, which raises body temperature. Intraperitoneal injections of peptone are widely used to induce fever in rats, and oral administration of EECC significantly decreased the rectal temperature of peptone-induced fever rats.  
Previous studies showed that EECC contains secondary metabolites like polyphenols, flavonoids, alkaloids, tannins, saponins, and triterpenes. Flavonoids have been reported to inhibit COX-2 enzyme activity, which reduces PGE2 synthesis and lowers fever.
In this RP–HPLC method, the linearity was within the range of 10–90 µg/mL, the method was successfully validated in the optimized conditions, and the validation parameters were within the limits. In this chromatographic method, the LOD and LOQ of atazanavir sulfate were found to be 0.09 µg/mL and 0.23 µg/mL, respectively. In the present investigation, atazanavir sulfate was subjected to its stability studies under different conditions as per the ICH guidelines.
From the neutral hydrolytic degradation study of atazanavir sulfate, it was found that no degradation took place over 4 h in neutral conditions.
The results of acidic hydrolysis showed degradation peaks at 4.77 min and 5.31 min along with the drug peak. The peak area showed that 51.62% of degradation of the drug occurred when the drug was kept in 0.1 M HCl at 80 °C up to 4 h.
Atazanavir sulfate upon alkaline degradation in 0.01 M NaOH at 80 °C up to 4 h underwent degradation, showing a degradation peak at 5.18 min in the chromatogram. The peak area of the drug showed that the percentage degradation is 30.64% in the above condition.
Atazanavir sulfate did not degrade after it was kept under direct sunlight for 21 days. No peak other than the drug peak was found in the chromatogram of that sample.
Atazanavir sulfate was not degraded after it was kept in the UV chamber for 48 h. In the oxidative degradation study, atazanavir sulfate showed no degradation after 4 h of exposure. The thermal degradation study showed that atazanavir sulfate was degraded when kept at 40 °C for 15 days. The degradant was retained at 7.29 min in the chromatogram along with the drug peak. The drug peak area showed that the degradation of the drug was 18.97%.
As cancer progresses, the TAMs in the TME adopt an immunosuppressive M2-like phenotype to support tumor growth. Targeting the macrophage phenotype to de-suppress the TME may enhance the response to immunotherapy. Recent studies have found that macrophages in the TME could switch from the immunosuppressive phenotype to the anti-tumor phenotype. It has been shown that, in addition to inducing tumor cell cycle arrest, paclitaxel skews TAMs toward the immune activity profile through Toll-like receptor 4 (TLR4), which might contribute to the anti-tumor effect of paclitaxel. The TLR4 agonist monophosphoryl lipid A combined with IFNg reprograms CD206+ TAMs to iNOS+ macrophages to kill cancer cells and activate T cells to control metastatic breast cancer and ovarian cancer in mice. These findings suggest that the state of macrophage polarization is important for the effective control of tumor progression, and that targeting macrophages to relieve the suppressive immune microenvironment may improve the efficacy of immunotherapy.
