Figure 2.

‘Pre‐onset’ PMX205 treatment at 9 mg·kg⁻¹·day⁻¹ in hSOD1^G93A transgenic mice. hSOD1^G93A mice were orally dosed with the selective C5a₁ receptor antagonist PMX205 at 35 days of age (9 mg·kg⁻¹·day⁻¹ in drinking water through to end‐stage). (A, left panel) A Kaplan–Meier plot of ages (in days) in which hSOD1^G93A mice treated with dH₂O (vehicle) or PMX205 reached end‐stage of disease (complete hindlimb paralysis and an inability to right itself once placed on its back (n = 13). * P < 0.05, significantly different from vehicle; log‐rank test. (A, right panel) The end‐stage survival age for each litter‐matched pair of vehicle‐ and PMX205‐treated hSOD1^G93A mice. (B) Body weight in vehicle‐ and PMX205‐treated hSOD1^G93A mice (n = 13). P > 0.05, significantly different from vehicle; two‐way ANOVA. (C) Hindlimb grip strength in hSOD1^G93A mice treated with either vehicle or PMX205 (n = 13) *P < 0.05, significantly different from vehicle; two‐way ANOVA with Fisher's LSD test at each age. (D) Disease progression (determined by age at which maximal grip strength decline at 25, 50, 75 and 100%) in hSOD1^G93A mice treated with PMX205 when compared with vehicle‐treated hSOD1^G93A mice at 25, 50, 75 and 100% decline in maximal grip strength (n = 13). * P < 0.05, significantly different from vehicle;two‐way ANOVA with Fisher's LSD test at each quartile. Data are expressed as mean ± SEM.