2. Metabolic Enzyme/Protease PI3K/Akt/mTOR Epigenetics
  3. 11β-HSD AMPK
  4. 11β-HSD1-IN-25

11β-HSD1-IN-25 is a selective and orally active 11β-HSD1 inhibitor. 11β-HSD1-IN-25 effectively reduces glucocorticoid levels in vitro and serum, and diminishes lipid accumulation in both vitro and vivo. 11β-HSD1-IN-25 modulates lipid metabolism through dual mechanisms: inhibition of 11β-HSD1 and activation of the AMP-activated protein kinase (AMPK) signaling pathway. 11β-HSD1-IN-25 can be used for obesity and related metabolic disorders research.

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11β-HSD1-IN-25

11β-HSD1-IN-25 Chemical Structure

CAS No. : 1261266-23-2

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11β-HSD1-IN-25 Related Antibodies

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Description

11β-HSD1-IN-25 is a selective and orally active 11β-HSD1 inhibitor. 11β-HSD1-IN-25 effectively reduces glucocorticoid levels in vitro and serum, and diminishes lipid accumulation in both vitro and vivo. 11β-HSD1-IN-25 modulates lipid metabolism through dual mechanisms: inhibition of 11β-HSD1 and activation of the AMP-activated protein kinase (AMPK) signaling pathway. 11β-HSD1-IN-25 can be used for obesity and related metabolic disorders research[1].

In Vitro

11β-HSD1-IN-25 (10 μM) suppresses 11β-HSD1 to ameliorate lipid metabolic disorders and reduces lipid accumulation in 3T3-L1 adipocytes[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

11β-HSD1-IN-25 Related Antibodies
In Vivo

11β-HSD1-IN-25 (0.5 mg/kg, p.o., daily for 60 days) alleviates obesity, reduces the size of adipocytes in adipose tissue, suppresses 11β-HSD1 to ameliorate adipose tissue lipid metabolic disorders, ameliorates adipocyte hypertrophy and inflammation in 11β-HSD1 lentivirus induced (or not)-male C57BL/6 mice[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: 11β-HSD1 lentivirus induced (or not) (i.v.)-male C57BL/6 mice (8 weeks, 20-22 g)[1]
Dosage: 0.5 mg/kg
Administration: p.o., daily for 60 days
Result: Significantly mitigated weight gain when induced by 11β-HSD1 lentivirus.
Significantly reduced serum concentrations of corticosterone (CORT), cholesterol (CHO), triglycerides (TG), low-density lipoprotein (LDL), and high density lipoprotein (HDL).
Improved adipocyte morphology.
Decreased 11β-HSD1 protein expression.
Exhibited a substantial increase in the protein expression levels of UCP1, the p-AMPK/AMPK ratio, and CPT1 when reduced by 11β-HSD1 lentivirus when reduced by 11β-HSD1 lentivirus.
Showed a significant reduction in the mRNA expression of Hsd11b1, Srebp1c, Fas, and Acc1 and exhibited a increase in the expression levels of Cpt1, Ucp1, and Hsl when reduced by 11β-HSD1 lentivirus.
Not exhibited a significant elevation in FAS protein expression in adipose tissue when not reduced by 11β-HSD1 lentivirus.
Resulted in a substantial reduction in FAS protein expression.
Upregulated HSL protein no matter reduced by 11β-HSD1 lentivirus or not.
Significantly reduced F4/80 protein expression in adipose tissue.
Molecular Weight

432.31

Formula

C21H12F8O
CAS No.
SMILES

O=C1/C(CC/C1=C\C2=C(C(F)(F)F)C=CC=C2F)=C/C3=C(C(F)(F)F)C=CC=C3F
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Purity & Documentation
References
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11β-HSD1-IN-25 Related Classifications

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Keywords:

11β-HSD1-IN-251261266-23-211β-HSDAMPK11beta-HSD11β-hydroxysteroid dehydrogenases11 beta-hydroxysteroid dehydrogenaseAMP-activated protein kinase11β-HSD1 inhibitorglucocorticoidlipid accumulationobesityInhibitorinhibitorinhibit

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