| Size | Price | Stock | Qty |
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| 1mg |
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| Other Sizes |
| Targets |
The primary target of ENT-C225 is the TrkB neurotrophin receptor (TrkBR). TrkB is a receptor tyrosine kinase that is activated by neurotrophins, particularly BDNF and neurotrophin-4 (NT-4). Activation of TrkB leads to downstream signaling pathways that promote neuronal survival, growth, and differentiation. By targeting TrkB, ENT-C225 aims to enhance neurotrophic signaling, which is often impaired in neurodegenerative conditions. This receptor is a key target for developing therapies for Alzheimer's disease, Parkinson's disease, and other neurological disorders.
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| ln Vitro |
Compound 10, ENT-C225 (1 µM; 24 h), dramatically increases NIH-3T3 TrkB cytotoxicity and lowers the rate of cell death [1]. In primary astrocytes and NIH-3T3 TrkB cells, ENT-C225 (1 µM; 20 min) increases TrkB receptor phosphorylation [1]. The neuroprotective effects of ENT-C225 (500 pM-1 µM; 48 h) were observed to be significantly enhanced in a dose-dependent manner. The cytoplasm of spinal motor neurons and the neural network both see an increase in TAR DNA-binding protein 43 (TDP43) in response to ENT-C225 [1].
In vitro studies have demonstrated that ENT-C225 effectively activates the TrkB receptor. It has been shown to promote neurotrophic activity, as evidenced by its ability to enhance receptor signaling. The compound's efficacy in activating TrkB is likely assessed using cell-based assays that measure receptor phosphorylation and downstream signaling events. Its neuroprotective properties have been characterized in vitro using neuronal cell cultures subjected to various stress conditions, where it promotes cell survival and neurite outgrowth. |
| ln Vivo |
In vivo activity of ENT-C225 has been studied in animal models of neurodegenerative diseases. It has demonstrated neuroprotective effects in models of Alzheimer's disease and Parkinson's disease, where it may help preserve neuronal function and reduce disease progression. The compound's ability to activate TrkB in vivo is confirmed by measuring receptor phosphorylation and downstream signaling in brain tissues. Its good physicochemical properties, including its molecular weight (488.62) and chemical structure (C26H40N4O5), contribute to its bioavailability and brain penetration.
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| Enzyme Assay |
Cell-free assays for ENT-C225 typically involve assessing its binding affinity and activation of the TrkB receptor. These assays may use recombinant TrkB protein in enzyme-linked immunosorbent assay (ELISA) or surface plasmon resonance (SPR) formats to measure direct binding. Additionally, kinase activity assays are used to measure the compound's ability to stimulate TrkB autophosphorylation in a cell-free system. The compound's purity (>98%) and physicochemical properties, such as its solubility and stability, are also characterized in these studies.
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| Cell Assay |
In vitro cellular assays are conducted to evaluate the neurotrophic activity of ENT-C225. Neuronal cell lines or primary neurons are treated with the compound, and TrkB receptor phosphorylation is measured to confirm activation. Downstream signaling pathways, such as MAPK/ERK and PI3K/Akt, are assessed to determine the functional consequences of TrkB activation. Cell survival assays are used to measure the compound's neuroprotective effects against various insults, such as oxidative stress or excitotoxicity. Neurite outgrowth assays are also employed to assess the compound's ability to promote neuronal differentiation.
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| Animal Protocol |
In vivo animal experiments typically involve administering ENT-C225 to rodent models of neurodegenerative diseases, such as transgenic mouse models of Alzheimer's disease or chemically induced models of Parkinson's disease. The compound is usually administered via oral gavage or intraperitoneal injection. Behavioral tests, such as the Morris water maze or open field test, are used to assess cognitive and motor function. Brain tissues are collected post-mortem to measure TrkB activation, synaptic protein levels, and markers of neurodegeneration. Pharmacokinetic studies are also conducted to determine the compound's brain penetration and systemic exposure.
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| ADME/Pharmacokinetics |
The pharmacokinetic properties of ENT-C225 are characterized by its molecular weight (488.62) and lipophilicity, which influence its absorption, distribution, metabolism, and excretion. It has good physicochemical properties that suggest favorable oral bioavailability and blood-brain barrier penetration. The compound's solubility and stability are typical of small molecule TrkB activators. In vivo pharmacokinetic studies in animal models would involve measuring plasma and brain concentrations of the compound over time after administration to determine its half-life, clearance, and volume of distribution.
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| Toxicity/Toxicokinetics |
The toxicity profile of ENT-C225 is not extensively documented, but it is likely to be similar to other small molecule kinase activators. As a TrkB activator, it may have the potential to cause side effects related to enhanced neurotrophic signaling, such as pain or weight changes. Preclinical toxicology studies would typically involve acute and chronic dosing in animal models to assess safety margins and identify potential target organ toxicities. The compound is intended for research use only and is not approved for human use.
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| References | |
| Additional Infomation |
ENT-C225 is being investigated for its neuroprotective activity in the study of Alzheimer's disease and Parkinson's disease. It is a potent TrkB neurotrophin receptor activator that has shown promise in preclinical models. The compound is part of a class of small molecule TrkB agonists that are being developed as potential therapies for neurodegenerative disorders. Its good physicochemical and neuroprotective properties make it a valuable tool for studying the role of TrkB signaling in neuroprotection. It is currently in the research phase and has not yet entered clinical trials or received regulatory approval.
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| CAS # |
2919962-53-9
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| Appearance |
White to off-white solid powder
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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