| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| 25mg |
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| 50mg | |||
| Other Sizes |
| Targets |
IC50: 2.9 μM (VDR)[1].
MeTC7 targets the vitamin D receptor (VDR). As an antagonist, it binds to VDR and inhibits its activity. VDR is a nuclear receptor that mediates the effects of vitamin D on calcium homeostasis, bone metabolism, immune function, and cell proliferation. By inhibiting VDR, MeTC7 modulates vitamin D signaling pathways. The compound shows potent VDR inhibitory activity with an IC₅₀ of 2.9 μM. It shows good antitumor effects. |
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| ln Vitro |
MeTC7 (compound 5) has an IC50 value of 2.9 μM, indicating strong VDR inhibitory activity[1]. The VDR-Ligand-binding domain in Silico is disrupted by MeTC7[1]. In the ovarian cancer cell-line, MeTC7 (250 nM; 18 h) decreases the expressions of Importin-4 and RXRα[1]. MeTC7 (250 nM; 18 h) causes PARP1 cleavage and reduces the viability of ovarian cancer cells[1].
In vitro, MeTC7 demonstrates potent VDR inhibitory activity with an IC₅₀ of 2.9 μM. It suppresses the viability of cancer cell lines. The compound is used in cell-based assays to investigate its effects on VDR-mediated signaling and cancer cell proliferation. Its activity in cellular assays modulates immune checkpoint expression. The compound's antitumor effects have been demonstrated in vitro. It is supplied for research purposes only. |
| ln Vivo |
MeTC7 (compound 5) (meTC7; 10 mg/kg) inhibits the growth of xenografts and spontaneous transgenic TH-MYCN neuroblastoma in vivo[1].
In vivo, MeTC7 reduces the growth of spontaneous transgenic TH-MYCN neuroblastoma and xenografts. These data demonstrate its in vivo antitumor efficacy. The compound is used in preclinical studies to evaluate its mechanism of action and potential as a therapeutic agent for cancer. Its ability to inhibit tumor growth in vivo supports its potential for cancer treatment. Specific dosing and efficacy data are not detailed in the available sources. |
| Enzyme Assay |
Non-cell-based enzyme/receptor binding assays for MeTC7 typically involve competitive binding studies using purified VDR protein. Standard protocols include incubating varying concentrations of the test compound with the VDR ligand-binding domain and a radiolabeled vitamin D ligand (e.g., [³H]-1,25(OH)₂D₃) in appropriate buffer systems, followed by separation of bound from free ligand via filtration or charcoal adsorption. Binding affinity (IC₅₀ values) is calculated using nonlinear regression analysis. The compound shows an IC₅₀ of 2.9 μM. Surface plasmon resonance (SPR) may also be employed.
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| Cell Assay |
Western Blot Analysis[1]
Cell Types: 2008 cells Tested Tested Concentrations: 250 nM Incubation Duration: 18, 12 h Experimental Results: diminished the expression of RXR-α, Importin-4 and increased cleaved PARP1 expression in 2008 cells. Cell Viability Assay[1] Cell Types: SKOV-3, IGROV-1, CAOV-3, OVCAR-3, OVCAR-8, and 2008 ovarian cancer cell-lines Tested Tested Concentrations: 0, 0.25, 0.5, 0.75, 1.0, 1.25 μM Incubation Duration: 24 h Experimental Results: diminished the viability of SKOV-3, IGROV-1, CAOV- 3, OVCAR-3, OVCAR-8, and 2008 ovarian cancer cell-lines. Cell-based assays for MeTC7 typically utilize cancer cell lines to evaluate its effects on cell viability and VDR-mediated signaling. Standard protocols involve culturing cells in appropriate media at 37°C in 5% CO₂, followed by treatment with varying concentrations of the compound (typically 0.1-100 μM) for 24-72 hours. Cell viability is assessed using MTT, CCK-8, or CellTiter-Glo assays. The compound suppresses the viability of cancer cell lines. Its effects on immune checkpoint expression (e.g., PD-L1) can also be studied. IC₅₀ values are calculated from dose-response curves. |
| Animal Protocol |
Animal/Disease Models: Mice[1]
Doses: 10 mg/kg Route of Administration: IP Experimental Results: decreased the growth of xenografts derived from ovarian cancer, medulloblastoma, and pancreatic cancer cells. Inhibited the growth of neuroblastoma cells and Xenografts. decreased MYCN expression and blocked the growth of TH-MYCN transgene-driven spontaneous neuroblastoma. In vivo animal studies for MeTC7 typically involve xenograft models or transgenic tumor models in mice. Standard protocols include subcutaneous implantation of cancer cells or use of spontaneous transgenic TH-MYCN neuroblastoma models, followed by administration of the compound via oral gavage, intraperitoneal injection, or intravenous injection at doses ranging from 1-50 mg/kg body weight. Tumor volume is measured twice weekly using calipers, and body weight is monitored for toxicity assessment. At study termination, tumors are collected for histopathological examination and biomarker analysis. All animal studies must comply with institutional ethical guidelines. |
| ADME/Pharmacokinetics |
Pharmacokinetic properties for MeTC7 are consistent with a small-molecule VDR antagonist. The compound has a molecular weight of 618.65 g/mol. For in vivo administration, formulations using suitable co-solvent systems may be employed. The compound should be stored as powder at -20°C for up to 3 years or in solvent at -80°C for 1 year. Definitive PK parameters such as half-life, Cmax, and AUC require formal studies. The compound is supplied for research purposes only.
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| References | |
| Additional Infomation |
MeTC7 is a vitamin D receptor (VDR) antagonist with potent VDR inhibitory activity (IC₅₀ = 2.9 μM) and good antitumor effects. It suppresses the viability of cancer cell lines and reduces the growth of spontaneous transgenic TH-MYCN neuroblastoma and xenografts in vivo. It modulates immune checkpoint expression such as PD-L1. Preclinical studies continue to evaluate its efficacy and mechanism of action for cancer treatment. It is not an approved drug and has not undergone clinical trials.
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| Molecular Formula |
C32H48BRN3O4
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|---|---|
| Molecular Weight |
618.645228385925
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| Exact Mass |
617.282
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| CAS # |
1817841-22-7
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| PubChem CID |
165437232
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| Appearance |
White to off-white solid powder
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| LogP |
8
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| Hydrogen Bond Donor Count |
0
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| Hydrogen Bond Acceptor Count |
4
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| Rotatable Bond Count |
8
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| Heavy Atom Count |
40
|
| Complexity |
1130
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| Defined Atom Stereocenter Count |
7
|
| SMILES |
BrCC(=O)O[C@H]1CC[C@@]2(C)C3(C1)C=CC1([C@@H]4CC[C@H]([C@H](C)CCCC(C)C)[C@@]4(C)CC[C@@H]12)N1C(N(C)C(N13)=O)=O
|
| InChi Key |
LBFDLJSQMPCWKK-YMNKQYQVSA-N
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| InChi Code |
InChI=1S/C32H48BrN3O4/c1-20(2)8-7-9-21(3)23-10-11-24-29(23,4)14-13-25-30(5)15-12-22(40-26(37)19-33)18-31(30)16-17-32(24,25)36-28(39)34(6)27(38)35(31)36/h16-17,20-25H,7-15,18-19H2,1-6H3/t21-,22+,23-,24-,25-,29-,30-,31?,32?/m1/s1
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| Chemical Name |
[(2R,5R,6R,9R,10R,13S)-6,10,18-trimethyl-5-[(2R)-6-methylheptan-2-yl]-17,19-dioxo-16,18,20-triazahexacyclo[13.5.2.01,9.02,6.010,15.016,20]docos-21-en-13-yl] 2-bromoacetate
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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) |
DMSO: 16.67 mg/mL (26.95 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 1.67 mg/mL (2.70 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 16.7 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.6164 mL | 8.0821 mL | 16.1642 mL | |
| 5 mM | 0.3233 mL | 1.6164 mL | 3.2328 mL | |
| 10 mM | 0.1616 mL | 0.8082 mL | 1.6164 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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