5-Hydroxyhexanoic acid
5-Hydroxyhexanoic acid is a normal monohydroxy carboxylic acid degradation product of
fatty acids with medium chain lengths (particularly hexanoic acid). 5-Hydroxyhexanoic acid functions as a predictor of early renal functional decline in type 2 diabetes with microalbuminuria.
For research use only. We do not sell to patients.
- CAS No.: 44843-89-2
- Formula: C6H12O3
- Molecular Weight:132.16
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Endogenous Metabolite Isoforms
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Biological Activity
Description
fatty acids with medium chain lengths (particularly hexanoic acid). 5-Hydroxyhexanoic acid functions as a predictor of early renal functional decline in type 2 diabetes with microalbuminuria[1].
In Vitro
5-Hydroxyhexanoic acid serves as a predictor of early renal function decline in type 2 diabetes mellitus with microalbuminuria, and its specificity is superior to that of urinary albumin excretion rate[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 44843-89-2
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Molecular Weight 132.16
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Formula C6H12O3
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SMILES
O=C(O)CCCC(O)C
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Structure Classification
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Initial Source
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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.
Protocols
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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
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)