ABR-238901 |
| Catalog No.GC63420 |
ABR-238901 est un bloqueur S100A8/A9 actif et puissant par voie orale et inhibe l'interaction S100A8/A9 avec ses récepteurs RAGE (récepteur pour les produits finaux de glycation avancée) et TLR4 (récepteur de type péage 4).
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 1638200-22-2
Sample solution is provided at 25 µL, 10mM.
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ABR-238901 is a newly developed blocker for S100A8/A9, which effectively inhibits the interaction between S100A8/A9 and the receptor for advanced glycation endproducts (RAGE) as well as toll-like receptor 4 (TLR4) [1-2].
ABR-238901(30 mg/kg；i.p) ameliorates septic cardiomyopathy in mice [3]. ABR-238901, administered at a dose of 10 mg/kg intraperitoneally, reduces neutrophil extracellular trap (NET) formation in abdominal sepsis by inhibiting S100A9[4]. In abdominal sepsis, ABR-238901 at doses of 30 mg/kg administered intraperitoneally reduced lung levels of MPO (a marker of neutrophil activation) by 74% [5]. In mice with multiple myeloma (MM), treatment with ABR-238901 at a dose of 30 mg/kg given orally daily for 5 days reduces angiogenesis in vivo[6]. Administering ABR-238901 at a dose of 30 mg/kg intraperitoneally for a short duration shifts the balance between inflammation and repair towards a reparatory environment in the ischemic myocardium [7].
References:
[1]. Zhu H, He M, et,al. Low-intensity pulsed ultrasound alleviates doxorubicin-induced cardiotoxicity via inhibition of S100a8/a9-mediated cardiac recruitment of neutrophils. Bioeng Transl Med. 2023 Jul 7;8(6):e10570. doi: 10.1002/btm2.10570. PMID: 38023700; PMCID: PMC10658545.
[2]. Mareş RG, Sabău AH, et,al. S100A8∕A9 is a valuable biomarker and treatment target to detect and modulate neutrophil involvement in myocardial infarction. Rom J Morphol Embryol. 2023 Apr-Jun;64(2):151-158. doi: 10.47162/RJME.64.2.04. PMID: 37518871; PMCID: PMC10520380.
[3]. Jakobsson G, Papareddy P, et,al. Therapeutic S100A8/A9 blockade inhibits myocardial and systemic inflammation and mitigates sepsis-induced myocardial dysfunction. Crit Care. 2023 Sep 29;27(1):374. doi: 10.1186/s13054-023-04652-x. PMID: 37773186; PMCID: PMC10540409.
[4]. Du F, Ding Z, et,al. S100A9 induces reactive oxygen species-dependent formation of neutrophil extracellular traps in abdominal sepsis. Exp Cell Res. 2022 Dec 15;421(2):113405. doi: 10.1016/j.yexcr.2022.113405. Epub 2022 Oct 31. PMID: 36328195.
[5]. Ding Z, Du F, et,al. Targeting S100A9 Reduces Neutrophil Recruitment, Inflammation and Lung Damage in Abdominal Sepsis. Int J Mol Sci. 2021 Nov 29;22(23):12923. doi: 10.3390/ijms222312923. PMID: 34884728; PMCID: PMC8658007.
[6]. De Veirman K, De Beule N, et,al. Extracellular S100A9 Protein in Bone Marrow Supports Multiple Myeloma Survival by Stimulating Angiogenesis and Cytokine Secretion. Cancer Immunol Res. 2017 Oct;5(10):839-846. doi: 10.1158/2326-6066.CIR-17-0192. Epub 2017 Sep 13. PMID: 28903971.
[7]. Marinković G, Koenis DS, et,al. S100A9 Links Inflammation and Repair in Myocardial Infarction. Circ Res. 2020 Aug 14;127(5):664-676. doi: 10.1161/CIRCRESAHA.120.315865. Epub 2020 May 21. PMID: 32434457.
Average Rating: 5 (Based on Reviews and 31 reference(s) in Google Scholar.)
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