TrkA
TrkA (tropomyosin receptor kinase A; encoded by NTRK1) is a high-affinity receptor tyrosine kinase for nerve growth factor (NGF) that regulates neuronal survival, differentiation, and sensory neuron function through ligand-induced receptor dimerization and autophosphorylation[1][2]. Mechanistically, NGF-TrkA signaling activates major downstream pathways including RAS/MAPK, PI3K/AKT, and PLCγ, thereby controlling transcriptional programs that support neuronal growth, maintenance, and synaptic function[1][2][3]. Through these signaling cascades, TrkA plays a central role in the development and maintenance of nociceptive neurons and contributes to neurotrophin-dependent cellular responses in the peripheral and central nervous systems[1][2]. In disease contexts, dysregulation of NGF/TrkA signaling has been implicated in chronic pain disorders and neurodegenerative conditions, including experimental models of Alzheimer's disease in which impaired TrkA signaling is associated with cholinergic neuronal dysfunction and synaptic deficits[3][4][5]. Compared with related neurotrophin receptors, TrkA is distinguished by its preferential activation by NGF, whereas TrkB primarily responds to BDNF and NT-4/5 and TrkC is activated predominantly by NT-3, enabling receptor-specific biological outcomes[6]. For experimental applications, both agonists and antagonists targeting the NGF-TrkA axis have been widely utilized to investigate neurotrophic signaling, neuronal survival mechanisms, and pain-related pathways, making TrkA an important molecular target in translational neuroscience research[4][5].
References:
- [1]. Norman BH, et al. Targeting the Nerve Growth Factor (NGF) Pathway in Drug Discovery. Potential Applications to New Therapies for Chronic Pain. J Med Chem. 2017 Jan 12;60(1):66-88. [Content Brief]
- [2]. Indo Y. NTRK1 Congenital Insensitivity to Pain with Anhidrosis. 2008 Aug 5 [updated 2020 Apr 30]. In: Adam MP, et al. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993–2026. PMID: 20301726. [Content Brief]
- [3]. Latina V, et al. Impaired NGF/TrkA Signaling Causes Early AD-Linked Presynaptic Dysfunction in Cholinergic Primary Neurons. Front Cell Neurosci. 2017 Mar 15;11:68. doi: 10.3389/fncel.2017.00068. PMID: 28360840; PMCID: PMC5350152. [Content Brief]
- [4]. Baño V, et al. Characterization and Structural Performance in Bending of CLT Panels Made from Small-Diameter Logs of Loblolly/Slash Pine. Materials (Basel). 2018 Nov 30;11(12):2436. [Content Brief]
- [5]. Mantyh PW, et al. Antagonism of nerve growth factor-TrkA signaling and the relief of pain. Anesthesiology. 2011 Jul;115(1):189-204. [Content Brief]
- [6]. Clinical Guidelines on the Identification, et al. National Institutes of Health. Obes Res. 1998 Sep;6 Suppl 2:51S-209S. Erratum in: Obes Res 1998 Nov;6(6):464. PMID: 9813653. [Content Brief]
-
TrkA Related Products (77)
Related Products (77)
-
Antibodies (4)
-
PF-06273340
0 ImagesPF-06273340 is a peripherally restricted pan-Trk inhibitor with IC50 values of 6, 4, 3 nM for TrkA, TrkB, and TrkC receptors. PF-06273340 binds in a DFG-out conformation, targeting less conserved kinase ligand binding domain regions outside the ATP binding pocket. PF-06273340 exhibits anti-hyperalgesic and analgesic effects. PF-06273340 can be used for the research of pain.
-
Zurletrectinib
0 ImagesSynonyms: ICP-723Zurletrectinib is a brain-penetrant, orally active TRK inhibitor (TRKA IC50 = 0.81 nM; TRKB IC50 = 0.145 nM; TRKC IC50 = 0.184 nM). Zurletrectinib exhibits stronger activity as a consequence of its augmented binding affinity for TRK kinases. Zurletrectinib exhibits higher activity against most TRK inhibitor resistance mutations (13 out of 18 mutations). Zurletrectinib can be used for the study of glioma.
-
CG428
0 ImagesCG428 is a potent and selective CRBN-dependent tropomyosin receptor kinase (TRK) PROTAC degrader that has anti-tumor activity. CG428 reduces levels of the tropomyosin 3 TPM3-TRKA fusion protein in KM12 colorectal carcinoma cells (DC50 = 0.36 nM) and inhibits downstream PLCγ1 phosphorylation (IC50 = 0.33 nM). CG428 has a higher binding affinity for TRKA than TRKB and TRKC (Kd = 1 nM, 28 nM and 4.2 nM, respectively). CG428 can be used for the research of colorectal carcinoma.
-
Udonitrectag
0 ImagesSynonyms: REC 0559Udonitrectag (REC 0559) is a nerve growth factor peptide mimetic and a TrkA receptor binder. Udonitrectag binds to the TrkA receptor, thereby mimicking anti-Apoptotic activity and corneal trophic activity. Udonitrectag promotes the healing of corneal epithelium and stroma. Udonitrectag is applicable to research related to neurotrophic keratitis.
-
TrkA-IN-1
0 ImagesCat. No.: HY-129634CAS No.: 1680179-43-4TrkA-IN-1 is a potent and selective Tropomyosin-related kinase A (TrkA) inhibitor with an IC50 of 99 nM in a cell-based assay. TrkA-IN-1 has analgesic activity.
-
CG428-NEG
0 ImagesCat. No.: HY-157542CAS No.: 2714560-39-9CG428-NEG is the negative control of PROTAC CG428 (HY-137465). CG428-NEG binds to TRKA, TRKB and TRKC with high affinity, with Kd values of 0.88 nM, 4.8 nM and 59.8 nM, respectively. CG428-NEG inhibits the growth of cancer cells and reduces the level of TPM3-TRKA fusion protein in cancer cells. CG428-NEG can be used in the research of colorectal cancer.
-
MNAC13
0 ImagesCat. No.: HY-P991622MNAC13 is a kind of mouse IgG1 chimeric antibody, targeting to human TrkA. MNAC13 inhibits the NGF dependent signaling pathway by specifically binding to TrkA receptors. MNAC13 has good analgesic effect and long-lasting efficacy. MNAC13 can be used for researches on inflammatory and chronic pain.
-
CZS-241
0 ImagesCat. No.: HY-149912CAS No.: 3016297-55-2CZS-241 is an orally active and selective inhibitor of Polo-like Kinase (PLK) 4 (IC50=2.6 nM). CZS-241 inhibits TRKA with an IC50 value of 2.74 μM. CZS-241 induces apoptosis and arrests cell cycle at S/G2 phase. CZS-241 shows highly potent antiproliferative activity against leukemia cell lines, and exhibits safety against normal cell lines.
-
Sitravatinib malate
0 ImagesCat. No.: HY-16961ACAS No.: 2244864-88-6Synonyms: MGCD516 malate; MG-516 malateSitravatinib malate (MGCD516 malate) is an orally bioavailable receptor tyrosine kinase (RTK) inhibitor with IC50s of 1.5 nM, 2 nM, 2 nM, 5 nM, 6 nM, 6 nM, 8 nM, 0.5 nM, 29 nM, 5 nM, and 9 nM for Axl, MER, VEGFR3, VEGFR2, VEGFR1, KIT, FLT3, DDR2, DDR1, TRKA, TRKB, respectively. Sitravatinib malate shows potent single-agent antitumor efficacy and enhances the activity of PD-1 blockade through promoting an antitumor immune microenvironment.
-
LPM4870108
0 ImagesCat. No.: HY-132229CAS No.: 2803679-07-2
-
FLT3/TrKA-IN-1
0 ImagesCat. No.: HY-146749FLT3/TrKA-IN-1 is a potent FLT3/TrKA dual kinase inhibitor with the IC50s of 43.8 nM, 97.2 nM, 92.5 nM and 23.6 nM for FLT3, FLT3-ITD, FLT3-TKD and TrKA, respectively. FLT3/TrKA-IN-1 induces cell cycle arrest at the G0/G1 phase as well as apoptosis and shows antiproliferative activity in vitro. FLT3/TrKA-IN-1 has the potential for the research of Acute myeloid leukemia (AML).
-
Fudotinib
0 ImagesCat. No.: HY-176942CAS No.: 2644645-39-4Synonyms: JYP0322Fudotinib (JYP0322) (ROS1-IN-3) is a potent orally active, selective, and CNS-penetrant ROS1 inhibitor. Fudotinib selectively inhibits human wild-type ROS1 and human ROS1G2032R with IC50s of 0.37 and 0.3 nM, respectively, showing 6-130-fold selectivity over TRKA, TRKB, and TRKC. Fudotinib inhibits proliferation of ROS1 fusion-expressing cells, and inhibits tumor growth in mouse xenograft models. Fudotinib can be used for the research of non-small cell lung cancer (NSCLC).
