BVT-2733 hydrochloride
Based on 4 publication(s) in Google Scholar
BVT-2733 hydrochloride is a potent, selective and orally active nonsteroidal 11β-HSD1 inhibitor. BVT-2733 hydrochloride is more potent against mouse 11β-HSD1 enzyme (IC50=96 nM) than against human 11β-HSD1 enzyme (IC50=3341 nM). BVT-2733 hydrochloride has the potential to be used in the study of arthritis and obesity-related diseases.
For research use only. We do not sell to patients.
- CAS No.: 376641-65-5
- Formula: C17H22Cl2N4O3S2
- Molecular Weight:465.42
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Please store the product under the recommended conditions in the Certificate of Analysis.
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Publications Citing Use of MedChemExpress (MCE) BVT-2733 hydrochloride
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Description
Chemical Information
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CAS No. 376641-65-5
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Molecular Weight 465.42
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Formula C17H22Cl2N4O3S2
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SMILES
O=S(C1=CC=CC(Cl)=C1C)(NC2=NC(CC(N3CCN(C)CC3)=O)=CS2)=O.Cl
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (4)
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Journal Impact Factor
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Most Recent
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Acta Pharm Sin B
2022 May;12(5):2358-2373. PMID: 35646525
BVT-2733 hydrochloride purchased from MedChemExpress. Usage Cited in: Acta Pharm Sin B. 2022 May;12(5):2358-2373. [Abstract]
Representative oil red O-stained images treated with BVT 2733 (10 μM).
BVT-2733 hydrochloride purchased from MedChemExpress. Usage Cited in: Acta Pharm Sin B. 2022 May;12(5):2358-2373. [Abstract]
Change curves of body weight treated with vehicle, 40 mg/kg EQST or 40 mg/kg BVT.2733, respectively.
BVT-2733 hydrochloride purchased from MedChemExpress. Usage Cited in: Acta Pharm Sin B. 2022 May;12(5):2358-2373. [Abstract]
11β-HSD1 and 11β-HSD2 enzyme activity in EQST or BVT.2733(40 mg/kg) treated 3T3-L1-derived mature adipocyte.
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Int J Biol Sci
The GR-gp78 Pathway is involved in Hepatic Lipid Accumulation Induced by Overexpression of 11β-HSD1. [Abstract]2022 Apr 30;18(8):3107-3121. PMID: 35637957
BVT-2733 hydrochloride purchased from MedChemExpress. Usage Cited in: Int J Biol Sci. 2022 Apr 30;18(8):3107-3121. [Abstract]
Western blot detection of proteins related to the lipid biosynthesis, oxidation, secretion, uptake, and hydrolysis pathways in 11β-HSD1 overexpressed or GFP overexpressed Hep1-6 cells exposed or not to 0.25 μM BVT2733.
BVT-2733 hydrochloride purchased from MedChemExpress. Usage Cited in: Int J Biol Sci. 2022 Apr 30;18(8):3107-3121. [Abstract]
Immunofluorescence staining of the distribution of GR (red) following treatment or not with 0.25 μM BVT2733 in Hep1-6 cells overexpressing 11β-HSD1 or GFP.
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J Ethnopharmacol
Glycyrrhizic acid and patchouli alcohol in Huoxiang Zhengqi attenuate intestinal inflammation and barrier injury via regulating endogenous corticosterone metabolism mediated by 11β-HSD1. [Abstract]2025 Feb 10;338(Pt 1):119025. PMID: 39489360 -
Mol Med Rep
11β‑hydroxysteroid dehydrogenase‑1 is associated with the activation of hepatic stellate cells in the development of hepatic fibrosis. [Abstract]2020 Oct;22(4):3191-3200. PMID: 32945429
Protocols
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Collagen-Induced Arthritis
Collagen-induced arthritis (CIA) is an autoimmune murine model of rheumatoid arthritis in which immunization with type II collagen (CII) emulsified in an adjuvant induces a T cell- and autoantibody-driven inflammatory arthritis characterized by synovial hyperplasia, immune cell infiltration, and joint destruction. The model typically relies on genetically susceptible mouse strains (e. g. , DBA/1) and reproduces key features of human rheumatoid arthritis, including anti-collagen immune responses and progressive joint inflammation. Disease onset generally occurs within ~3-4 weeks after immunization, depending on antigen/adjuvant combinations and protocol variation. The immunopathology is driven by adaptive immune activation against CII, leading to systemic and local joint inflammation mediated by pro-inflammatory cytokines and effector immune cells, making CIA a standard preclinical platform for evaluating immunomodulatory and anti-arthritic interventions.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Purity & Documentation
References
[1]. 11β-hydroxydehydrogenase 1 (11β-HSD1) Inhibitor in Development
[2]. Zhang L, et al. 11β-Hydroxysteroid dehydrogenase 1 inhibition attenuates collagen-induced arthritis. Int Immunopharmacol. 2013 Nov;17(3):489-94. [Content Brief]
[3]. Wang L, et al. BVT.2733, a selective 11β-hydroxysteroid dehydrogenase type 1 inhibitor, attenuates obesity and inflammation in diet-induced obese mice. PLoS One. 2012;7(7):e40056. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
BVT-2733 hydrochloride Related Classifications
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