| Size | Price | Stock | Qty |
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| 1mg |
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| Other Sizes |
| Targets |
The primary targets are P-type (Cav2.1) and Q-type (Cav2.1) voltage-gated calcium channels. omega-Conotoxin MVIIC also blocks N-type calcium channels, but with lower affinity compared to its action on P/Q types. By binding with high affinity to these channels, the toxin prevents the calcium influx that is critical for triggering the fusion of synaptic vesicles and the subsequent release of neurotransmitters, such as glutamate.
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| ln Vitro |
The signal in LLC/luc and MDA-MB-231/luc cells treated with AkaLumine HCl peaked at a lower concentration (2.5 μM), while D-luciferin and CycLuc1 produced more bioluminescence at higher doses. rise, even at 250 μM not reaching the maximum signal [1].
At a concentration of 1-5 uM, omega-Conotoxin MVIIC TFA significantly and potently suppresses the inhibition of glutamate release mediated by another agent, 11-keto-beta-boswellic acid (AKBA), demonstrating its ability to block P/Q-type calcium channel function. Its primary activity is the potent and reversible blockade of P/Q-type calcium currents in isolated neurons, with an IC50 typically in the low micromolar range. |
| ln Vivo |
Compared to the injection of D-luciferin, AkaLumine hydrochloride demonstrated an 8.1-fold increase in the signal from lung metastases. Bioluminescence of mice treated with CycLuc1 and AkaLumine HCl was measured 15 minutes after intravenous injection of LLC/luc cells at a concentration of 5 mM (maximum dose) in order to assess the advantage of AkaLumine HCl over CycLuc1 in detecting deep tissue targets. Photographs for contrast CycLuc1 has a low solubility in water, which contributes to its increased concentration. When it comes to detecting disseminated lung cancer cells, AkaLumine hydrochloride outperforms CycLuc1 by a factor of 3.3. By imaging the same mice that had lung metastases following intraperitoneal injection of 5 mM substrate in the order of CycLuc1 and AkaLumine hydrochloride, and every 8 hours in the opposite order, the superiority of AkaLumine hydrochloride was further established. visualize. When comparing AkaLumine hydrochloride to CycLuc1, the lung metastatic signal is almost four times higher [1].
Due to its potent neurotoxic effects, omega-Conotoxin MVIIC is not suitable for systemic therapeutic use. However, it is used as an investigative tool in vivo. For example, when injected intrathecally (into the spinal cord) in rodent pain models, P/Q-type channel blockers can produce antinociceptive (pain-relieving) effects, providing evidence for the role of these channels in pain transmission at the spinal cord level. |
| Enzyme Assay |
The radiolabeled peptide (e.g., ¹2⁵I-labeled omega-Conotoxin MVIIC) is used in standard radioligand binding assays. Membranes prepared from mammalian brain tissue (e.g., rat cerebellum, which is rich in P/Q-type channels) are incubated with the radiolabeled toxin in the presence or absence of varying concentrations of unlabeled omega-Conotoxin MVIIC TFA. After incubation, the mixture is rapidly filtered through glass fiber filters to separate bound from free ligand, and the radioactivity is measured using a scintillation counter to determine binding affinity (Kd) and competition.
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| Cell Assay |
omega-Conotoxin MVIIC is used to study neurotransmitter release from primary neuronal cultures (e.g., rat cortical or hippocampal neurons). The neurons are cultured in multi-well plates. The cells are treated with omega-Conotoxin MVIIC (e.g., 1-10 uM) and then depolarized with a high potassium buffer. The amount of neurotransmitter (e.g., glutamate or GABA) released into the culture supernatant is quantified by ELISA or high-performance liquid chromatography (HPLC). The toxin's ability to inhibit release is measured and compared to controls.
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| Animal Protocol |
In an intrathecal injection mouse model for pain, adult male ICR mice are used. A baseline pain response (e.g., thermal paw withdrawal latency) is measured. omega-Conotoxin MVIIC TFA (e.g., 10-100 pmol) is then administered via intrathecal injection in a volume of 5 uL. At various time points post-injection (e.g., 15, 30, 60 min), the pain response is re-assessed. An increase in paw withdrawal latency indicates an analgesic effect. The compound's effect is compared to a vehicle (saline) control group.
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| ADME/Pharmacokinetics |
As a peptide neurotoxin, omega-Conotoxin MVIIC does not have classic pharmacokinetic properties associated with small molecule drugs. It is not orally bioavailable and has a very short half-life in circulation due to rapid degradation by proteases. Its action is typically studied ex vivo or upon direct, localized injection into the central nervous system (e.g., intrathecal or intracerebroventricular administration).
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| Toxicity/Toxicokinetics |
The TFA salt of omega-Conotoxin MVIIC is a potent neurotoxin and is considered toxic. It is for research use only and is not intended for human use. Its toxicity is due to its mechanism of action: blocking P/Q-type calcium channels at the presynaptic nerve terminal, preventing neurotransmitter release. This can lead to severe neuronal dysfunction, paralysis, and respiratory failure if the toxin reaches the systemic circulation or central nervous system.
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| References |
[1]. Cheng Wei Lu, et al. 11-Keto-β-Boswellic Acid Attenuates Glutamate Release and Kainic Acid-Induced Excitotoxicity in the Rat Hippocampus. Planta Med. 2020 Apr;86(6):434-441.
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| Additional Infomation |
omega-Conotoxin MVIIC is a research-grade peptide used as a pharmacological tool to dissect the roles of different voltage-gated calcium channel subtypes in neuronal physiology. It is particularly useful in distinguishing between N-type and P/Q-type channel function in neurotransmission. As a toxin, it is not a drug candidate for systemic administration. It has been invaluable in developing our understanding of synaptic transmission and in identifying calcium channels as targets for pain therapy.
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| Appearance |
Typically exists as solid at room temperature
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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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