Name | BT-11 |
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Description | BT-11 is an orally available LANCL2 binding compound for treating inflammatory bowel disease. |
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Related Catalog | |
In Vitro | LANCL2 engagement produces an increase of PKA, followed by an accumulation of cAMP in the cytoplasm. BT-11 treatment splenocytes shows a dose−response increase of cAMP production. BT-11 stimulates cAMP production by activating the LANCL2 pathway[1]. |
In Vivo | The oral treatment with BT-11 (8 mg/kg/d) in a mouse model of inflammatory bowel disease results in lowering the disease activity index, decreasing colonic inflammatory lesions by 4-fold, and suppressing inflammatory markers (e.g., TNF-α, and interferon-γ) in the gut. Furthermore, studies in LANCL2−/− mice demonstrates that loss of LANCL2 abrogates beneficial actions of BT-11, suggesting high selectivity for the target. Oral treatment with BT-11 (8 mg/kg/day) ameliorates colitis in mice. Initial safety assessment in rats indicates that oral treatment with BT-11 at high doses has an excellent safety profile up to 1000 mg/kg/day[1]. BT-11 is well tolerated in rats, and may hold promise as an orally active therapeutic for Crohn’s disease. One hour after oral administration of a single dose of 80 mg/kg, BT-11 has a maximal concentration of 21 ng/mL; the half-life is 3 hours[2]. |
Animal Admin | Rats: Male Harlan Sprague Dawley rats are treated with a single oral dose of 500 mg/kg and 80 mg/kg/d for 14 days. Treated and control rats are observed for behavioral detriments, and blood and tissues are collected for clinical pathology and histopathological examination[2]. Mice: Wild type and LANCL2−/− male mice are treated with 8 mg/kg/d BT-11 over 8 weeks. Mice are sacrificed and spleens are collected for splenocytes isolation. Cell lysates are collected and cAMP intracellular concentration is measured[1]. |
References |
Molecular Formula | C30H24N8O2 |
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Molecular Weight | 528.2 |
Appearance | white solid |
Storage condition | -20℃ |