PMX 205 is an effective complement antagonist of the C5a receptor.

In the MTT assay, in 24 h plate, it shows that all groups are significant when compared with negative control group. For the PMX 205 group, the value recorded is between 0.09893 to 0.2465, EP54 group, 0.02724 to 0.1748, and Tamoxifen group, the value recorded in between 0.09880 to 0.2464. Only one group shows a significant result for the 72 h plate, PMX 205 (antagonist group) with the value recorded in between 0.02136 to 0.5322. Only two groups show a significant result for the 48 h plate of incubation time, which are PMX 205 and Tamoxifen. The values recorded are between 0.04987 to 0.3273 and 0.5777 to 0.8551 respectively [1].

PMX 205 (1 mg/kg/day; SOD1G93A rats; p.o.) from two-time points (days 28 and 70) before the onset of major clinical symptoms. Both treatment groups have a significant extension in survival time compared with untreated rats (p=0.022, day 28; p=0.015, day 70), with no clear differences in outcomes between the two treatment regimens. PMX 205-treated animals also display reduced levels of astroglial proliferation in the lumbar spinal cord. Animals treated with PMX 205 (1 mg/kg/day, oral) show a significant extension of survival time and a reduction in end-stage motor scores, as compared with vehicle-treated rats. Tg2576 mice are treated with PMX 205 (PMX205) at 20 μg/mL in the drinking water (n=17) from 12 to 15 mo of age, the time frame at which there is a rapid accumulation of amyloid deposits in these animals. Untreated Tg2576 animals (n=11) are used as controls. After 3 mo, animals treated with PMX 205 show significantly less fibrillar plaque load (thioflavine reactivity) than do untreated animals. PMX 205 also significantly reduces hyperphosphorylated tau (69%) in 3×Tg mice [2][3].