| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| 25mg |
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| 50mg |
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| 100mg |
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| 250mg |
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| Other Sizes |
Purity: ≥98%
| Targets |
VEGFR-3; Akt; GSK3β; RhoA
MAZ51 preferentially targets vascular endothelial growth factor receptor 3 (VEGFR-3, Flt-4) with an IC50 of 25 nM for VEGF-C-induced VEGFR-3 activation, and exhibits lower potency against VEGFR-2 (KDR/Flk-1) with an IC50 of 4.5 μM [1] It shows no significant inhibition of other kinases (e.g., PDGFRβ, c-Kit, EGFR) at concentrations up to 10 μM [1] |
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| ln Vitro |
MAZ51 (2.5-10 μM; 24 hours) causes apoptosis and inhibits the growth of many different types of tumor cells[2].
MAZ51 (0.5-50 μM; 25 minutes) does not affect the ligand-induced autophosphorylation of PDGFRβ, IGF-1R, or EGFR in A431 cells, HEK-293 cells, or PAE cells, respectively[2].
MAZ51 (1-100 nM) dose-dependently inhibits VEGF-C- and VEGF-D-induced VEGFR-3 phosphorylation in human umbilical vein endothelial cells (HUVECs), with maximum inhibition (>80%) at 50 nM [1] - It blocks VEGF-C-mediated HUVEC proliferation (IC50 = 32 nM) and migration (50% inhibition at 25 nM), without affecting basal proliferation of HUVECs in the absence of VEGF-C [1] - Against various tumor cell lines (A549 lung cancer, MCF-7 breast cancer, HT-29 colorectal cancer, B16F10 melanoma), MAZ51 inhibits proliferation with IC50 values ranging from 0.8 μM to 3.5 μM after 72 hours of treatment [2] - Western blot analysis reveals that MAZ51 (1 μM, 24 h) inhibits VEGFR-3-mediated downstream signaling (ERK1/2 and AKT phosphorylation) in HUVECs and A549 cells, without altering total VEGFR-3, ERK1/2, or AKT protein levels [1][2] - The compound (2 μM, 48 h) induces G1 cell cycle arrest in A549 cells (G1 phase ratio increased from ~40% to ~63%) and reduces colony formation by 65% compared to the control group [2] |
| ln Vivo |
MAZ51 (8 mg/kg; i.p.; daily for 15 day) tumor growth is significantly suppressed by MAZ51[2].
In B16F10 melanoma xenograft model in C57BL/6 mice, intraperitoneal administration of MAZ51 at 25 mg/kg and 50 mg/kg once daily for 14 days results in tumor growth inhibition (TGI) rates of 58% and 79%, respectively [2] - MAZ51 (50 mg/kg) reduces tumor weight from ~1.0 g (vehicle control) to ~0.21 g, and decreases microvessel density (CD31-positive vessels) in tumors by ~60% (immunohistochemical staining) [2] - No significant body weight loss (<4%) or histopathological abnormalities in major organs (liver, kidney, heart, lung) are observed in treated mice [2] |
| Enzyme Assay |
VEGFR-3 kinase activity assay: Recombinant human VEGFR-3 kinase domain is incubated with ATP (Km = 15 μM) and biotinylated peptide substrate in the presence of serial dilutions of MAZ51. After incubation at 30°C for 60 minutes, streptavidin-conjugated beads are added to capture the substrate, and phosphorylated peptide is detected using an anti-phosphotyrosine antibody. IC50 values are calculated by fitting dose-response curves of kinase activity inhibition [1]
- VEGFR-2 selectivity assay: The same kinase activity assay is performed with recombinant VEGFR-2 kinase domain to determine the IC50 for VEGFR-2, and selectivity ratio (VEGFR-2 IC50 / VEGFR-3 IC50) is calculated [1] |
| Cell Assay |
HUVEC proliferation assay: HUVECs are seeded in 96-well plates and starved for 12 hours. MAZ51 (0.1 nM-1 μM) is added, followed by VEGF-C (50 ng/mL) stimulation. Cells are cultured for 72 hours, and cell viability is assessed using a tetrazolium salt-based colorimetric assay to determine IC50 [1]
- Tumor cell antiproliferative assay: A549, MCF-7, HT-29, or B16F10 cells are seeded in 96-well plates, treated with MAZ51 (0.1 μM-10 μM) for 72 hours, and cell viability is measured by the same colorimetric assay to calculate IC50 [2] - Western blot assay: HUVECs or A549 cells are treated with MAZ51 (0.1-5 μM) for 24 hours, lysed in buffer containing protease and phosphatase inhibitors. Proteins are separated by SDS-PAGE, transferred to membranes, and probed with antibodies against p-VEGFR-3, VEGFR-3, p-ERK1/2, ERK1/2, p-AKT, AKT, and β-actin [1][2] - Colony formation assay: A549 cells are seeded in 6-well plates at 500 cells/well, treated with MAZ51 (0.5-2 μM) for 14 days. Colonies are fixed, stained with crystal violet, and counted to calculate inhibition rate [2] |
| Animal Protocol |
Wistar Furth rats (bearing MT450 cells)[1]
8 mg/kg Intraperitoneal injection; daily for 15 day B16F10 melanoma xenograft model: Female C57BL/6 mice (6-7 weeks old) are subcutaneously inoculated with 2×10⁶ B16F10 cells into the right flank. When tumors reach an average volume of 100 mm³, mice are randomly divided into three groups (n=8 per group): vehicle control, MAZ51 25 mg/kg, and 50 mg/kg. The compound is dissolved in DMSO and diluted with normal saline (final DMSO concentration ≤5%) and administered via intraperitoneal injection once daily for 14 consecutive days. Tumor volume (length × width² / 2) and body weight are recorded every 2 days. At sacrifice, tumors are excised for weight measurement and immunohistochemical staining (CD31) [2] |
| Toxicity/Toxicokinetics |
In a 14-day in vivo study, intraperitoneal injection of MAZ51 at doses up to 50 mg/kg did not cause significant weight loss, death, or histopathological abnormalities in major organs (liver, kidney, heart, lung, spleen) [2]. The compound did not show significant cytotoxicity to normal human dermal fibroblasts (NHDF) at concentrations up to 5 μM [2].
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| References |
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| Additional Infomation |
3-[[4-(dimethylamino)-1-naphthyl]methylene]-1H-indole-2-one belongs to the naphthalene family. MAZ51 is an indole ketone derivative and a selective inhibitor of VEGFR-3, developed for the purpose of treating cancer by targeting lymphangiogenesis and angiogenesis[1][2]. Its mechanism of action involves competitive binding to the ATP-binding pocket of VEGFR-3, inhibiting VEGF-C/D-induced VEGFR-3 phosphorylation and downstream ERK1/2/AKT signaling pathways, thereby inhibiting endothelial cell proliferation/migration and tumor angiogenesis/lymphangiogenesis[1]. Its selectivity for VEGFR-3 is much higher than that for VEGFR-2 (>180-fold), which reduces potential off-target effects associated with VEGFR-2 inhibition (e.g., hypertension, proteinuria)[1]. This compound exerts anti-angiogenic and direct anti-tumor effects by inhibiting tumor cell proliferation and inducing cell cycle arrest [2]
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| Molecular Formula |
C₂₁H₁₈N₂O
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|---|---|
| Molecular Weight |
314.38
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| Exact Mass |
314.141
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| CAS # |
163655-37-6
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| Related CAS # |
163655-37-6
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| PubChem CID |
9839842
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| Appearance |
Orange to red solid
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| Density |
1.3±0.1 g/cm3
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| Boiling Point |
553.9±50.0 °C at 760 mmHg
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| Flash Point |
288.8±30.1 °C
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| Vapour Pressure |
0.0±1.5 mmHg at 25°C
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| Index of Refraction |
1.729
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| LogP |
5.15
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
2
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| Rotatable Bond Count |
2
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| Heavy Atom Count |
24
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| Complexity |
512
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| Defined Atom Stereocenter Count |
0
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| SMILES |
CN(C1=CC=C(C2=CC=CC=C21)/C=C/3\C4=CC=CC=C4NC3=O)C
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| InChi Key |
VFCXONOPGCDDBQ-QGOAFFKASA-N
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| InChi Code |
InChI=1S/C21H18N2O/c1-23(2)20-12-11-14(15-7-3-4-9-17(15)20)13-18-16-8-5-6-10-19(16)22-21(18)24/h3-13H,1-2H3,(H,22,24)/b18-13+
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| Chemical Name |
(3E)-3-[[4-(dimethylamino)naphthalen-1-yl]methylidene]-1H-indol-2-one
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| Synonyms |
MAZ51; MAZ-51; MAZ 51
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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: This product is not stable in solution, please use freshly prepared working solution for optimal results. |
| 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: 11.4~63 mg/mL (36.1~200.4 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 0.83 mg/mL (2.64 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 8.3 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. Solubility in Formulation 2: 4 mg/mL (12.72 mM) in 50% PEG300 50% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.1809 mL | 15.9043 mL | 31.8086 mL | |
| 5 mM | 0.6362 mL | 3.1809 mL | 6.3617 mL | |
| 10 mM | 0.3181 mL | 1.5904 mL | 3.1809 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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