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. 2022 May 5;122(8):1314–1325. doi: 10.1055/a-1759-9962

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The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. ( https://creativecommons.org/licenses/by-nc-nd/4.0/ )

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License, which permits unrestricted reproduction and distribution, for non-commercial purposes only; and use and reproduction, but not distribution, of adapted material for non-commercial purposes only, provided the original work is properly cited.

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Fig. 1 — Nonanticoagulated mice 24 hours after experimental ICH. (A) Hemorrhage volume and (B) representative DAB staining images showing hemorrhage volume of wild-type ( WT ) mice treated with saline and CM-352 under no anticoagulation. (C) Functional evaluation (pole test). (D) Hemorrhage volume and (E) functional evaluation (Bederson's test) in WT- and MMP-10-deficient ( Mmp10 −/− ) mice. Treatment: CM-352 (1 mg/kg). Mean ± SD, * p < 0.05 vs. saline; ^# p < 0.05 vs. basal; ^†† p < 0.01 vs. WT , using the Kruskal–Wallis and Mann–Whitney U-test, n ≥ 9 /group. ICH, intracranial hemorrhage; SD, standard deviation.