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Discover high-quality research tools to investigate GLP-1 mechanisms and next-generation metabolic targets.
OBESITY RESEARCH SOLUTIONSCiliary neurotrophic factor (CNTF) is a member of the IL-6 superfamily of cytokines.1,2 It is a class-I helical cytokine that contains binding sites for a complex of CNTF receptor α (CNTFRα), glycoprotein 130 (gp130), and leukemia inhibitor factor receptor β (LIFRβ).1 CNTF is expressed in the brain, eyes, bone, and liver, as well as in spinal cord glial cells, astrocytes, Schwann cells, and skeletal muscle. It is involved in neuroprotection, neuroinflammation, neurogenesis, metabolism, and bone remodeling and primarily signals through the JAK/STAT pathway. Recombinant CNTF induces neurite outgrowth in chick embryonic dorsal root ganglion neurons and increases neuron survival in chick embryonic ciliary ganglia in vitro.3 Homozygous knockout of Cntf decreases facial motor neuron number and forelimb grip strength in mice.4 CNTF also decreases body weight, food intake, and serum insulin levels in ob/ob mice.5 Serum levels of CNTF are increased in patients with amyotrophic lateral sclerosis (ALS).6 Cayman’s CNTF (human, recombinant) protein can be used for cell-based assays. This protein consists of 214 amino acids and has a calculated molecular weight of 24.5 kDa.
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1. Ciliary neurotrophic factor (CNTF): New facets of an old molecule for treating neurodegenerative and metabolic syndrome pathologies. Cytokine Growth Factor Rev. 26(5), 507-515 (2015).
2. Cytokines of the LIF/CNTF family and metabolism. Cytokine 82, 122-124 (2016).
3. Recombinant human and rat ciliary neurotrophic factors. J. Neurochem. 57(3), 1003-1012 (1991).
4. Disruption of the CNTF gene results in motor neuron degeneration. Nature 65(6441), 27-32 (1993).
5. Ciliary neurotrophic factor corrects obesity and diabetes associated with leptin deficiency and resistance. Proc. Natl. Acad. Sci. U S A 94(12), 6456-6461 (1997).
6. Serum level of CNTF is elevated in patients with amyotrophic lateral sclerosis and correlates with site of disease onset. Eur. J. Neurol. 15(4), 355-359 (2008).