SB 290157

01/01/2020 - "We conclude that SB290157 is safe and effective with and without late IVT following TE stroke. "
01/01/2020 - "We used two different models of TE stroke to examine the efficacy of SB290157 alone and in combination with late IVT. "
01/01/2020 - "We hypothesized SB290157 would confer neuroprotection in TE stroke with and without "late" IVT. "
01/01/2020 - "SB290157 remains untested in thromboembolic (TE) models, which better approximate human stroke and also facilitate testing in combination with IVT. "
01/01/2019 - "We conclude that the C3aR antagonist, SB 290157, may be used in the future to limit the neuronal death by limiting secondary phagocytosis after stroke."

01/01/2021 - "Pharmacological targeting of the complement C3a receptor using SB290157 alleviated PDGF-D-induced neuroinflammation by blocking macrophage polarization and inhibited pathological choroidal neovascularization. "
10/01/2020 - "Notably, C3a receptor antagonist SB290157 trifluoroacetate attenuated LPS-induced hippocampal neuroinflammation and inhibitory synapse related protein loss, contributing to improved cognitive function. "

01/01/2020 - "In a photothrombotic (PT) stroke model, which exhibits rapid spontaneous reperfusion, SB290157 given at 1 hr post-PT significantly improved neurofunction and reduced infarction at 48 hr. In an embolic (eMCAo) model, SB290157 administered at 2 hr improved histological and functional outcomes. "

04/01/2019 - "In this study, we used an in vitro model of ischemia (oxygen glucose deprivation; OGD) to investigate the protective effect of a C3aR antagonist (C3aRA, SB290157) on brain endothelial cells (bEnd.3). "

10/17/2023 - "SB290157 confers a potential therapeutic approach for renin-dependent hypertension-induced kidney injury."
01/01/2019 - "The C3a receptor inhibitor SB-290157 attenuated the hypertension caused by Abelcet and decreased the BP thereafter. "
10/17/2023 - "Treatment with the C3aR antagonist SB290157 significantly mitigated the effect of renin induction of C3aR expression and alleviated renin-dependent hypertension-induced tubulointerstitial fibrosis by improving PPARα/CPT-1α-mediated Mito FAO in TECs, as well as inhibiting tubular profibrotic phenotype transition. "