| Size | Price | Stock | Qty |
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| 1mg |
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| 5mg |
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| 10mg |
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| 25mg | |||
| Other Sizes |
| Targets |
KB: ~100 nM (CRF2 receptor)[2] EC50: 140 nM (CRF1 receptor)[2]
α-Helical CRF(9-41) TFA targets the CRF1 and CRF2 receptors, which are key components of the hypothalamic-pituitary-adrenal (HPA) axis involved in stress responses. CRF1 receptors are primarily involved in the stress response and anxiety, while CRF2 receptors are involved in appetite regulation and stress coping. The compound acts as a competitive antagonist for the CRF2 receptor with a KB of approximately 100 nM, blocking the binding of endogenous CRF and preventing receptor activation. It serves as a partial agonist for the CRF1 receptor with an EC50 of 140 nM, meaning it can activate the receptor but with lower efficacy than the full agonist. This dual activity makes the compound a valuable tool for studying the differential roles of CRF1 and CRF2 receptors in stress-related behaviors and disorders. |
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| ln Vitro |
In vitro, α-helical CRF(9-41) TFA acts as a competitive CRF2 receptor antagonist with a KB of approximately 100 nM and as a partial agonist for the CRF1 receptor with an EC50 of 140 nM. These activities are assessed in cell-free receptor binding assays and cellular functional assays. The compound is used to study CRF receptor signaling pathways, including cAMP accumulation and receptor internalization. In neuroscience research, it is used to investigate the role of CRF receptors in stress, anxiety, and addiction. The compound's α-helical structure is critical for its receptor binding and activity.
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| ln Vivo |
In vivo, α-helical CRF(9-41) TFA reverses nicotine-induced conditioned anxiety in animal models. This demonstrates its role in modulating stress-related behaviors and its potential for studying anxiety disorders and addiction. The compound is typically administered via intracerebroventricular injection to bypass the blood-brain barrier and deliver the peptide directly to the central nervous system. In these studies, behavioral assays such as conditioned place preference or elevated plus maze are used to assess anxiety-like behaviors. The compound's ability to reverse nicotine-induced anxiety suggests that CRF receptors are involved in the anxiogenic effects of nicotine withdrawal.
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| Enzyme Assay |
Cell-free receptor binding assays for α-helical CRF(9-41) TFA involve incubating the compound with CRF1 or CRF2 receptor preparations in buffer, measuring displacement of radiolabeled CRF, and calculating binding affinity. The compound has a KB of approximately 100 nM for the CRF2 receptor. For functional assays, the compound's ability to activate or inhibit receptor signaling is measured using cAMP accumulation assays or other downstream readouts. The compound's EC50 for the CRF1 receptor is 140 nM. These assays are used to characterize the compound's pharmacological profile and to study CRF receptor signaling pathways.
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| Cell Assay |
Cellular assays for α-helical CRF(9-41) TFA involve treating CRF receptor-expressing cells with the compound and measuring functional readouts such as cAMP accumulation, calcium flux, or receptor internalization. For CRF1 receptor partial agonism, the compound's ability to stimulate cAMP production is measured and compared to the full agonist CRF. For CRF2 receptor antagonism, the compound's ability to block CRF-induced cAMP production is measured. These assays are used to study CRF receptor signaling and to evaluate the compound's activity in cellular systems.
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| Animal Protocol |
Animal studies for α-helical CRF(9-41) TFA involve administering the compound to rodents via intracerebroventricular injection. The compound reverses nicotine-induced conditioned anxiety in animal models. In these studies, behavioral assays such as conditioned place preference, elevated plus maze, or open field test are used to assess anxiety-like behaviors. The compound's effects on stress-related behaviors are evaluated, and its potential for treating anxiety disorders and addiction is investigated. The compound's ability to cross the blood-brain barrier is limited, necessitating direct central administration.
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| ADME/Pharmacokinetics |
Pharmacokinetic data for α-helical CRF(9-41) TFA are limited. As a peptide with a molecular weight of approximately 3.5 kDa, it has poor oral bioavailability and limited blood-brain barrier penetration. The compound is typically administered intracerebroventricularly to achieve central nervous system exposure. When administered via this route, the peptide is expected to have a short half-life due to rapid enzymatic degradation. Comprehensive pharmacokinetic studies have not been performed, as the compound is primarily a research tool rather than a drug candidate. For research purposes, the compound is typically handled as a peptide and not administered systemically for pharmacokinetic profiling.
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| Toxicity/Toxicokinetics |
Toxicological data for α-helical CRF(9-41) TFA are limited. Standard safety precautions for handling peptides apply, including the use of personal protective equipment such as gloves and safety goggles. The compound should be handled in a well-ventilated area, and contact with skin and eyes should be avoided. The TFA salt form may cause irritation. The compound is not classified as a carcinogen or mutagen based on available data, but comprehensive toxicological evaluation has not been performed. As with all research chemicals, it should be handled with care and used only in accordance with safety guidelines.
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| References |
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| Additional Infomation |
α-Helical CRF(9-41) TFA is a research peptide, not an approved drug. It has no clinical trial or marketing approval status for therapeutic use. The compound acts as a competitive antagonist for the CRF2 receptor with a KB of approximately 100 nM and as a partial agonist for the CRF1 receptor with an EC50 of 140 nM. It reverses nicotine-induced conditioned anxiety in animal models. The compound is used in neuroscience research to study CRF receptor function and stress-related disorders. Its α-helical structure is critical for its receptor binding and activity. The compound is typically administered intracerebroventricularly and is supplied as a TFA salt.
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| Molecular Formula |
C168H275F3N46O55S2
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| Molecular Weight |
3940.42
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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 Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
| 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) |
H2O :~1.82 mg/mL (~0.46 mM)
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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.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 0.2538 mL | 1.2689 mL | 2.5378 mL | |
| 5 mM | 0.0508 mL | 0.2538 mL | 0.5076 mL | |
| 10 mM | 0.0254 mL | 0.1269 mL | 0.2538 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
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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