S-Adenosylmethionine (SAM) and S-Adenosylhomocysteine (SAH) ELISA Combo Kit

S-Adenosylmethionine (SAM) and  S-Adenosylhomocysteine (SAH)  ELISA Combo Kit
  • Detection sensitivity limit of 0.2 µM SAH and 0.625 nM SAM
  • Suitable for use with plasma, serum, lysates, and other biological fluid samples
  • SAH and SAM standards included

 

Video: Color Development in an ELISA

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S-Adenosylmethionine (SAM) and S-Adenosylhomocysteine (SAH) ELISA Combo Kit
Catalog Number
MET-5151-C
Size
96 assays
Detection
Colorimetric
Manual/Data Sheet Download
SDS Download
Price
$840.00
Product Details

S-adenosylmethionine (SAM) is a substrate for methyl transfers to various biomolecules that yields S-adenosylhomocysteine (SAH). SAH is then hydrolyzed to homocysteine and adenosine, which is converted to methionine, and ultimately back to SAM. SAH can act as a methylation inhibitor, therefore the SAM/SAH ratio, or methylation potential, is important for maintaining proper methylation in the cell.

Our S-Adenosylmethionine (SAM) and  S-Adenosylhomocysteine (SAH)  ELISA Combo Kit is designed for detection and quantitation of both SAM and SAH in plasma, serum, lysates, or biological fluid samples. This assay is a competitive ELISA where samples and an anti-SAM or anti-SAH antibody are added to a plate coated with a SAM or SAH conjugate. The sample and conjugate compete for antibody binding, which generates a reverse curve.  Samples with high SAM and SAH levels will bind the majority of the antibody, which gets washed away and results in a low OD, while samples with low SAM and SAH levels will leave more antibody available to bind to the conjugate, producing a high signal.

Recent Product Citations
  1. Dai, J. et al. (2025). NNMT promotes acquired EGFR-TKI resistance by forming EGR1 and lactate-mediated double positive feedback loops in non-small cell lung cancer. Mol Cancer. 24(1):79. doi: 10.1186/s12943-025-02285-y.
  2. Samorì, E. et al. (2025). Influence of feeding time on daily rhythms of locomotor activity, clock genes, and epigenetic mechanisms in the liver and hypothalamus of the European sea bass (Dicentrarchus labrax). Fish Physiol Biochem. 51(1):50. doi: 10.1007/s10695-025-01461-7.
  3. Moreno Rueda, L.Y. et al. (2025). Single-cell analysis of neoplastic plasma cells identifies myeloma pathobiology mediators and potential targets. Cell Rep Med. 6(2):101925. doi: 10.1016/j.xcrm.2024.101925.
  4. Mahendran, G. et al. (2024). Multi-Omics Approach Reveals Genes and Pathways Affected in Miller-Dieker Syndrome. Mol Neurobiol. doi: 10.1007/s12035-024-04532-7.
  5. Shelp, G.V. et al. (2024). Exposure to prenatal excess or imbalanced micronutrients leads to long-term perturbations in one-carbon metabolism, trimethylamine-N-oxide and DNA methylation in Wistar rat offspring. FASEB J. 38(16):e70032. doi: 10.1096/fj.202401018RR.
  6. Chen, T.Y. et al. (2024). Mitochondrial S-adenosylmethionine deficiency induces mitochondrial unfolded protein response and extends lifespan in Caenorhabditis elegans. Aging Cell. 23(4):e14103. doi: 10.1111/acel.14103.
  7. Kadam, I. et al. (2023). Associations between nutrients in one-carbon metabolism and fetal DNA methylation in pregnancies with or without gestational diabetes mellitus. Clin Epigenet. 15:137. doi: 10.1186/s13148-023-01554-1.
  8. Rajabian, N. et al. (2023). Methionine adenosyltransferase2A inhibition restores metabolism to improve regenerative capacity and strength of aged skeletal muscle. Nat Commun. 14(1):886. doi: 10.1038/s41467-023-36483-3.