hIL23A/hIL12B

通过hIL12B(NM-HU-2000057)与hIL23A(NM-HU-18030)小鼠交配获得。

Fig.1 Detection of hIL23 and mIL23 expression in serum by ELISA (n=2). 

Abbr. HO, homozygous; WT, wild type.

Note. hIL23A/hIL12B and C57BL/6 mice were i.p. injected with LPS.

Table.1 Blood chemistry examination in 6-week-old HO/HO hIL23A/hIL12B mice (n=3 /group).

Table.2 Blood routine examination in 6-week-old HO/HO hIL23A/hIL12B mice (n=3 /group).

Fig.2 In vivo efficacy evaluation of anti-IL23 (Risankizumab, 20mpk, i.p., Q3D) and anti-IL23/IL12 (Ustekinumab, 20mpk, i.p., Q3D) in imiquimod (IMQ)-induced psoriasis model in hIL23A/hIL12B mice (3-6 mice/group, 6 weeks, female). IMQ treatment induced body weight loss in female hIL23A/hIL12B mice. Neither Risankizumab nor Ustekinumab treatment alleviated this weight loss, with both antibody-treated groups showing final body weight reductions.

Fig.3 In vivo efficacy evaluation of anti-IL23 (Risankizumab, 20mpk, i.p., Q3D) and anti-IL23/IL12 (Ustekinumab, 20mpk, i.p., Q3D) in imiquimod (IMQ)-induced psoriasis model in hIL23A/hIL12B mice (3-6 mice/group, 6 weeks, female). IMQ treatment successfully induced psoriasis-like skin inflammation in female hIL23A/hIL12B mice, characterized by increased skin thickness and elevated PASI scores (including erythema and scaling) over the 7-day observation period. Notably, Risankizumab demonstrated better therapeutic effect than Ustekinumab in lleviating IMQ-induced psoriasis.