• Product name

  • Detection method

  • Precision

    Sample n Mean SD CV%
    Overall 12 4.5%
    Sample n Mean SD CV%
    Overall 3 5.8%
  • Sample type

    Cell culture extracts, Tissue Extracts
  • Assay type

    Sandwich (quantitative)
  • Sensitivity

    2 ng/ml
  • Recovery

    Sample specific recovery
    Sample type Average % Range
    Serum 104 95% - 118%
    Cell culture media 105 97% - 114%

  • Assay duration

    Multiple steps standard assay
  • Species reactivity

    Reacts with: Mouse, Rat, Human
  • Product overview

    ab129734 Medium-chain-acyl-CoA dehydrogenase (MCAD, gene ACADM) ELISA (Enzyme-Linked Immunosorbent Assay) kit is an in vitro enzyme-linked immunosorbent assay for the accurate quantitative measurement of medium-chain-acyl-CoA dehydrogenase in human, rat and mouse tissue and cell culture extracts. The assay employs an ACADM specific antibody coated onto well plate strips. Standards and samples are pipetted into the wells and ACADM present in the sample is bound to the wells by the immobilized antibody. The wells are washed and a primary anti-ACADM detector antibody is added. After washing away unbound detector antibody, an HRP-conjugated secondary detector antibody (HRP Label) specific for the primary detector antibody is pipetted to the wells. The wells are again washed, a TMB substrate solution is added to the wells and color develops in proportion to the amount of ACADM bound. The developing blue color is measured at 600 nm. Optionally the reaction can be stopped by adding hydrochloric acid which changes the color from blue to yellow and the intensity can be measured at 450 nm.

    MCAD (medium-chain acyl-CoA dehydrogenase), encoded by the ACADM gene, is an oxidoreductase enzyme of the mitochondrial fatty acid beta-oxidation pathway that is specific for acyl chain lengths of 4 to 16. MCAD utilizes the electron transfer flavoprotein (ETF) as an electron acceptor that transfers the electrons to the main mitochondrial respiratory chain via ETF-ubiquinone oxidoreductase (ETF dehydrogenase).

  • Tested applications

    Suitable for: ELISAmore details
  • Platform




Our Abpromise guarantee covers the use of ab129734 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
ELISA Use at an assay dependent concentration.


  • The graph above shows an experiment to determine the levels of ACADM encoded protein in various fibroblast cell lines. Three Medium Chain Acyl-CoA Dehydrogenase Deficient (MCADD) patient fibroblast cell lines (P1-3) each harboring the common MCAD mutation K304E (984A>G in ACADM gene) were analyzed. Each patient cell line shows significant reduction in ACADM protein expression when compared to control adult fibroblast cells from three unaffected individuals (CON1-3).
  • Example of serially titrated ACADM protein in the assay working range.



This product has been referenced in:

  • Koster KL  et al. Functional studies of 18 heterologously expressed medium-chain acyl-CoA dehydrogenase (MCAD) variants. J Inherit Metab Dis N/A:N/A (2014). ELISA ; Human . Read more (PubMed: 24966162) »
See 1 Publication for this product

Customer reviews and Q&As


Vielen Dank für Ihre Antwort.

Leider ist mir bei meiner letzten Antwort ein Fehler unterlaufen und ich möchte diesen hiermit korrigieren:

ab110296 wird nicht im Kit ACADM ELISA Kit (ab129734) verwendet.. Es wird ein Antikörper verwendet, der nicht einzeln erhältlich ist. Bitte entschuldigen Sie vielmals diese Fehlinformation.

Bezüglich der anderen Fragen habe ich unsere Spezialisten bei MitoSciences gefragt. Ich habe ihnen die Antwort direkt unten rein kopiert:

"We purchased the cell line with the K304E (984A>G in ACADM gene) from the Coriell repository. The cell line is homozygous for 984A>G . The mutation in this cell line was found with a decrease in MCAD activity (12% from control) by the submitter, but there is no specific reference for this particular cell line in the coriell website.


However, it is well known in the literature that the K304E aa change (homozygous or compound heterozygous) induces MCAD deficiency (measured by enzyme activity). References below. Many of these studies were done before there were commercially available MCAD antibodies. So the WB data does not exist. Therefore we tested the above cell line from Coriell with our antibody 3B7BH7 and found that MCAD protein levels are significantly decreased (both by WB and by ICC). The customer can look at the data in the ICE booklet as mentioned in my previous email. We don’t have WB data with the antibody used in the kit showing control vs deficient, because the antibody is WB negative.

A good place to look at mutations known to induce MCAD deficiency is OMIM.


http://omim.org/entry/201450#reference32 reported the findings in a prospective neonatal screening program in Pennsylvania using tandem mass spectrometry. From the first 80,371 newborns screened, they found 9 babies with MCAD (1/8930), plus 2 additional newborns, screened because of a previously known family history. Molecular analysis showed that 56% of the patients were compound heterozygotes for the 985A-G mutation (K304E; http://omim.org/entry/607008#0001), commonly referred to as G985, and a second mutation.

In 9 patients with MCAD deficiency, http://omim.org/entry/201450#reference16 found a 985A-G transition which resulted in a lys304-to-glu substitution (K304E; http://omim.org/entry/607008#0001) in the mature protein. These patients were unrelated, suggesting a high incidence of this abnormality among Caucasian patients. The change was not found in 20 healthy Caucasian and 6 healthy Japanese subjects. http://omim.org/entry/201450#reference16 found this point mutation in 31 of 34 (91%) mutant MCAD alleles. http://omim.org/entry/201450#reference31 estimated that 90% of MCAD cases involve the same mutation.

http://omim.org/entry/201450#reference33 characterized the molecular defect in 4 patients with mild MCAD deficiency. In routine neonatal screening on the fifth day of life, they had been found to have abnormal acylcarnitine profiles indicative of MCAD deficiency. Two were of German origin and the other 2 were born to different consanguineous Turkish parents. In all 4, the clinical course and routine laboratory investigations up to the age of 6 months were unremarkable. Enzyme studies showed residual MCAD activities between those with classic MCAD deficiency and heterozygotes. In 2 cases, ACADM gene analysis revealed compound heterozygosity for the common K304E mutation (http://omim.org/entry/607008#0001) and the 199T-C mutation (Y42H; http://omim.org/entry/607008#0011), which they designated Y67H. In the 2 children of consanguineous parents, homozygosity was found for the gly267-to-arg mutation (G267R; http://omim.org/entry/607008#0003) and the S220L mutation (http://omim.org/entry/607008#0012), respectively. As in other metabolic disorders, the distinction between 'normal' and 'disease' in MCAD deficiency is blurred into a spectrum of enzyme deficiency states caused by different mutations in the ACADM gene potentially influenced by factors affecting intracellular protein processing."

Ich hoffe, diese Information ist hilfreich und wird Ihnen Ihre Bedenken bezüglich des Kits nehmen.

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