Member of the neurotrophin growth factor family that binds and activates TrkB and p75 neurotrophin receptors. Enhances the survival, growth and differentiation of neurons. BDNF expression is altered in neurodegenerative disorders such as Parkinson's and Alzheimer's disease.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solubility||Soluble in water|
Preparing Stock Solutions
The following data is based on the product molecular weight 26984. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||0.04 mL||0.19 mL||0.37 mL|
|5 mM||0.01 mL||0.04 mL||0.07 mL|
|10 mM||0 mL||0.02 mL||0.04 mL|
|50 mM||0 mL||0 mL||0.01 mL|
References are publications that support the biological activity of the product.
Lipsky and Marini (2007) Brain-derived neurotrophic factor in neuronal survival and behavior-related plasticity. Ann.N.Y.Acad.Sci. 1122 130 PMID: 18077569
Evans and Barker (2008) Neurotrophic factors as a therapeutic target for Parkinson's disease. Expert Opin.Ther.Targets 12 437 PMID: 18348680
Wang et al (2008) The when and where of BDNF and the antidepressant response. Biol.Psychiat. 63 640
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Keywords: BDNF (human), BDNF (human) supplier, activators, TrkB, p75, receptors, Neurotrophin, Receptors, Receptor, Tyrosine, Kinases, RTKs, Trk, 2837, Tocris Bioscience
5 Citations for BDNF (human)
Citations are publications that use Tocris products. Selected citations for BDNF (human) include:
Zhong et al (2015) BDNF interacts with endocannabinoids to regulate cocaine-induced synaptic plasticity in mouse midbrain dopamine neurons. Mol Pain 35 4469 PMID: 25762688
Parsons et al (2014) Bidirectional control of postsynaptic density-95 (PSD-95) clustering by Huntingtin. J Biol Chem 289 3518 PMID: 24347167
Hossaini et al (2010) Nociceptive stimulation induces expression of Arc/Arg3.1 in the spinal cord with a preference for neurons containing enkephalin. Cell Metab 6 43 PMID: 20653942
Chiara et al (2010) Brain-derived neurotrophic factor controls cannabinoid CB1 receptor function in the striatum. J Neurosci 30 8127 PMID: 20554863
Li et al (2011) Synergistic activation of dopamine D1 and TrkB receptors mediate gain control of synaptic plasticity in the basolateral amygdala. PLoS One 6 e26065 PMID: 22022509
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Major depressive disorder is characterized by depressed mood and a loss of interest and/or pleasure. Updated in 2015 this poster highlights presynaptic and postsynaptic targets for the potential treatment of major depressive disorder, as well as outlining the pharmacology of currently approved antidepressant drugs.
Huntington's Disease Poster
Huntington's disease (HD) is a monogenic neurodegenerative disorder, which is characterized by the prevalent loss of GABAergic medium spiny neurons (MSN) in the striatum. This poster summarizes the MSN intracellular signaling pathways implicated in the pathology of HD, as well as highlighting the use of iPSCs for HD modeling.
Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.
Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.