Key Features and Values
– Unique mAbs developed against specific linear epitopes
– Specific to human AMH (associated form)
– Complementary AMH products available
– Automation ready
The picoAMH (Anti-Müllerian hormone) enzyme linked immunuosorbent assay (ELISA) kit provides materials for the quantitative measurement of ultra-low concentrations of AMH in human serum and other biological fluids. This assay is intended for in vitro diagnostic use.
Anti-Müllerian hormone (AMH), a member of the TGFβ superfamily, is a homodimeric glycoprotein composed of two 55 kDa N-terminal and two 12.5 kDa C-terminal homodimers, non-covalently linked by disulfide bridges.
Recent studies have shown that the AMH C-terminal homodimer is much less active than the noncovalent complex, but almost all activity can be restored by associating with the N-terminal pro-region, which reforms a complex with the mature C-terminal homodimer. This finding raises the possibility that the AMH noncovalent complex is the active form of protein. It was reported that the cleaved AMH noncovalent complex binds to AMHRII and stimulates intracellular signaling, whereas full-length AMH shows only minimal activity1.
AMH is secreted by the Sertoli cells in males. During embryonic development, AMH is responsible for Müllerian duct regression. AMH continues to be produced by the testes until puberty and then decreases slowly to residual post-puberty values. In females, AMH is produced by the granulosa cells of small growing follicles from the 36th week of gestation onwards until menopause when levels become undetectable. Potential clinical applications of low end anti-müllerian hormone (AMH) have been published in premature ovarian insufficiency2, ovarian tumors3-4, menopause5-7 and many more.
1. di Clemente et al. Mol Endocrinol, November 2010, 24 (11): 2193-2206.
2. Méduri G, et. Al.Hum Reprod. 2007;22:117-23.
3. Lee M, Donahoe et al. Journal of Clinical Endocrinology and Metabolism 1996; 81:571-575.
4. Anderson R.A et al. Human Reproduction 2006, Vol.21 (10): 2583–2592.
5. Robertson, D.M et al. Menopause 2014 Dec;21(12):1277-1286.
6. Freeman EW, et al. 2012. J Clin Endocrinol Metab;97:1673-1680.
7. Tehrani FR, et al. J Clin Endocrinol Metab 2013;98:729–735.