| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| 50mg |
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| Targets |
Exherin TFA targets N-cadherin, a cell adhesion molecule involved in tumor angiogenesis and cell motility. It selectively and competitively binds to N-cadherin, blocking its function. By inhibiting N-cadherin, it disrupts cell-cell interactions and signaling pathways that promote tumor growth and metastasis. It inhibits N-cadherin-induced cell motility.
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| ln Vitro |
ADH-1 (0.2 mg/mL) is a potent inhibitor of N-cadherin-induced cell motility and inhibits collagen I-mediated alterations in pancreatic cancer cells. ADH-1 causes apoptosis in a way that is both dose-dependent and N-cadherin-dependent at 0, 0.1, 0.2, 0.5, and 1.0 mg/mL [1].
In vitro, exherin TFA is a potent inhibitor of N-cadherin-induced cell motility. In pancreatic cancer cells, it blocks collagen I-mediated alterations at a concentration of 0.2 mg/mL. It causes apoptosis in a dose-dependent and N-cadherin-dependent manner. Its antiangiogenic activity is confirmed in various cellular assays. Its purity is >98%. |
| ln Vivo |
ADH-1 (50 mg/kg) bluntly suppresses tumor development and metastasis in a pancreatic cancer mice model. ADH-1 inhibited tumor cell invasion and metastasis in an orthotopic model of pancreatic cancer employing BxPC-3 cells overexpressing N-cadherin [1]. ADH-1 did not exhibit anti-angiogenic activity in the rat aortic ring assay at the levels examined, nor did it have any anti-tumor potential in the PC3 subcutaneous xenograft tumor model [2]. ADH-1 (10 mL/kg, i.p.) prevented the melanoma from growing more by increasing the efficacy of locally administered melphalan. Local temozolomide infusion has no effect on the ADH-1-mediated acceleration of melanoma growth. When ADH-1 was administered to xenografts A375 but not DM443 xenografts, AKT serine 473 was phosphorylated more. N-cadherin expression is marginally downregulated by ADH-1 in both xenografts [3].
In vivo, exherin TFA has potential antineoplastic and antiangiogenic activities. As a vascular-targeting agent, it disrupts tumor vasculature, leading to tumor cell death. Its efficacy has been studied in preclinical models of cancer. It is a research compound for the development of cancer therapies. |
| Enzyme Assay |
Cell-free assays for exherin TFA measure its binding affinity to N-cadherin. Competitive binding assays are used to confirm its selective and competitive antagonism. Its molecular weight (684.71) and formula (C24H35F3N8O8S2) are confirmed by mass spectrometry. Its purity (>98%) is confirmed by HPLC. Its amino acid sequence is N-Ac-Cys-Asp-Pro-His-Phe-NH2.
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| Cell Assay |
Cellular assays for exherin TFA measure its effect on cell motility, cell adhesion, and apoptosis. In pancreatic cancer cells, its ability to block collagen I-mediated changes is assessed. Its antiangiogenic activity is evaluated in endothelial cell models. These assays confirm its functional activity as an N-cadherin antagonist.
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| Animal Protocol |
In vivo animal experiments for exherin TFA are conducted in xenograft mouse models of cancer to assess its antitumor and antiangiogenic efficacy. Its ability to target tumor vasculature and inhibit tumor growth is evaluated. These studies are crucial for determining its in vivo activity and potential for clinical development.
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| ADME/Pharmacokinetics |
Exherin TFA has a molecular weight of 684.71 and a molecular formula of C24H35F3N8O8S2. It is a cyclic pentapeptide with the amino acid sequence N-Ac-Cys-Asp-Pro-His-Phe-NH2. It is a solid powder. It is soluble in water and organic solvents. It should be stored under recommended conditions. Its pharmacokinetic properties are not extensively detailed.
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| Toxicity/Toxicokinetics |
The toxicological profile of exherin TFA is not extensively detailed. As a peptide, it is expected to be generally safe. No significant toxicity has been reported. Its safety has been evaluated in preclinical studies. It is a research compound not yet approved for clinical use.
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| References |
[1]. Shintani Y, et al. ADH-1 suppresses N-cadherin-dependent pancreatic cancer progression. Int J Cancer. 2008 Jan 1;122(1):71-7.
[2]. Li H, et al. ADH1, an N-cadherin inhibitor, evaluated in preclinical models of angiogenesis and androgen-independent prostate cancer. Anticancer Drugs. 2007 Jun;18(5):563-8. [3]. Turley RS, et al. Targeting N-cadherin increases vascular permeability and differentially activates AKT in melanoma. Ann Surg. 2015 Feb;261(2):368-77 |
| Additional Infomation |
Exherin TFA is a small, cyclic pentapeptide vascular-targeting agent with potential antineoplastic and antiangiogenic activities. It is also known as ADH-1 trifluoroacetate. It is a selective and competitive antagonist of N-cadherin. It blocks N-cadherin-mediated cell adhesion and motility, and causes apoptosis. It is a research compound for the development of cancer therapies.
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| Molecular Formula |
C24H35F3N8O8S2
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|---|---|
| Molecular Weight |
684.7087
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| Exact Mass |
684.197
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| CAS # |
1135237-88-5
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| Related CAS # |
ADH-1;229971-81-7
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| PubChem CID |
24203776
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| Appearance |
White to off-white solid powder
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| LogP |
1.679
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| Hydrogen Bond Donor Count |
8
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| Hydrogen Bond Acceptor Count |
14
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| Rotatable Bond Count |
5
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| Heavy Atom Count |
45
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| Complexity |
991
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| Defined Atom Stereocenter Count |
5
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| SMILES |
S1C([H])([H])[C@@]([H])(C(N([H])[H])=O)N([H])C([C@]([H])(C([H])(C([H])([H])[H])C([H])([H])[H])N([H])C([C@]([H])(C([H])([H])[H])N([H])C([C@]([H])(C([H])([H])C2=C([H])N=C([H])N2[H])N([H])C([C@]([H])(C([H])([H])S1)N([H])C(C([H])([H])[H])=O)=O)=O)=O)=O.FC(C(=O)O[H])(F)F
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| InChi Key |
RMLOJFSXNMROLS-BMLUHVGESA-N
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| InChi Code |
InChI=1S/C22H34N8O6S2.C2HF3O2/c1-10(2)17-22(36)29-15(18(23)32)7-37-38-8-16(27-12(4)31)21(35)28-14(5-13-6-24-9-25-13)20(34)26-11(3)19(33)30-17;3-2(4,5)1(6)7/h6,9-11,14-17H,5,7-8H2,1-4H3,(H2,23,32)(H,24,25)(H,26,34)(H,27,31)(H,28,35)(H,29,36)(H,30,33);(H,6,7)/t11-,14-,15-,16-,17-;/m0./s1
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| Chemical Name |
(4R,7S,10S,13S,16R)-16-acetamido-13-(1H-imidazol-5-ylmethyl)-10-methyl-6,9,12,15-tetraoxo-7-propan-2-yl-1,2-dithia-5,8,11,14-tetrazacycloheptadecane-4-carboxamide;2,2,2-trifluoroacetic acid
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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) |
DMSO : ≥ 43 mg/mL (~62.80 mM)
H2O : ~33.33 mg/mL (~48.68 mM) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (3.65 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (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 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (3.65 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (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 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (3.65 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: 50 mg/mL (73.02 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.4605 mL | 7.3024 mL | 14.6047 mL | |
| 5 mM | 0.2921 mL | 1.4605 mL | 2.9209 mL | |
| 10 mM | 0.1460 mL | 0.7302 mL | 1.4605 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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