| Size | Price | Stock | Qty |
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| Targets |
Aurora A 45 nM (IC50)
CD532 targets Aurora A kinase, a key regulator of mitosis that is overexpressed in many cancers. The compound inhibits Aurora A with an IC50 of 45 nM. It breaks the native conformation of Aurora-A and drives the degradation of N-Myc in N-Myc-driven cancers. CD532 also inhibits several CDKs, FGFRs, MEKs, and PDGFRs. The compound has the dual role of blocking Aurora A kinase activity and driving MYCN degradation. |
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| ln Vitro |
In MYCN-amplified neuroblastoma cell lines SK-N-BE(2) and Kelly, CD532 (1-10000 nM; 72 h) is cytotoxic, with EC50s of 223.2 nM and 146.7 nM, respectively[1]. MYCN protein in SK-N-BE(2) cells is lost in a dose-dependent manner upon exposure to CD532 (0.1–1 μM; 24 h)[1]. SK-N-BE(2) cells are prevented from entering S-phase by CD532 (1 μM; 6 h)[1].
In vitro studies demonstrate that CD532 (1-10000 nM; 72 h) is cytotoxic, with EC50 values of 223.2 nM and 146.7 nM. The compound inhibits Aurora A kinase with an IC50 of 45 nM. It breaks the native conformation of Aurora-A, drives the degradation of N-Myc, and exhibits anti-proliferative effects. CD532 also inhibits several CDKs, FGFRs, MEKs, and PDGFRs. |
| ln Vivo |
In mice with subcutaneous sonic hedgehog (SHH)-subtype medulloblastoma, CD532 (25 mg/kg; ip twice weekly for 3 weeks) reduces the tumor volume and improves survival[1]. MYCN-amplified neuroblastoma xenografts produce less MYCN protein when treated with CD532 (60 mg/kg; intraperitoneally for two days)[1]. In mice, CD532 (20 mg/kg; ip) exhibits an AUC0-24 of 27 μM·h and a serum half-life of approximately 1.5 hours[1].
In vivo, CD532 drives the degradation of N-Myc in N-Myc-driven cancers and exhibits anti-proliferative effects. The compound has the dual role of blocking Aurora A kinase activity and driving MYCN degradation. It is used in cancer research. Further studies would be needed to fully evaluate its efficacy in various cancer models. |
| Enzyme Assay |
The Aurora A inhibitory activity of CD532 can be assessed using in vitro kinase assays. In a typical assay, recombinant Aurora A kinase is incubated with a peptide substrate, ATP (including radiolabeled ³³P-ATP), and varying concentrations of CD532. The incorporation of phosphate into the substrate is measured, and the IC50 is calculated. The IC50 for Aurora A inhibition is 45 nM. The compound's ability to drive MYCN degradation can be assessed by Western blotting.
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| Cell Assay |
Cell Viability Assay[1]
Cell Types: SK-N-BE(2) and Kelly cells Tested Concentrations: 1, 10, 100, 1000, 10000 nM Incubation Duration: 72 hrs (hours) Experimental Results: Inhibited the cell viability of SK-N-BE(2) and Kelly cells, with EC50s of 223.2 nM and 146.7 nM, respectively. Cell Cycle Analysis[1] Cell Types: SK-N-BE(2) cells Tested Concentrations: 1 μM Incubation Duration: 4 hrs (hours) Experimental Results: Resulted in a rapid and potent loss of S-phase and accumulation in both G0/G1 and G2. Western Blot Analysis[1] Cell Types: SK-N-BE(2) cells Tested Concentrations: 0.1, 0.25, 0.5, 1 μM Incubation Duration: 2, 4, 6, 24 hrs (hours) Experimental Results: Causes dose-dependent and time-dependent loss of MYCN protein. The cellular activity of CD532 is assessed using cancer cell lines, particularly N-Myc-driven cancer cells. Cells are treated with escalating concentrations of CD532 (1-10000 nM; 72 h). Cell viability is measured using MTT or CellTiter-Glo assays, and EC50 values are calculated. Aurora A inhibition is assessed by measuring Aurora A activity or phosphorylation of its substrates. MYCN degradation is assessed by Western blotting. Cell cycle analysis is performed using flow cytometry. |
| Animal Protocol |
Animal/Disease Models: Homozygous nu/nu (nude) mice with SHH-subtype MYCN-expressing medulloblastoma[1]
Doses: 25 mg/kg Route of Administration: Ip twice weekly for 3 weeks Experimental Results: diminished the level of MYCN protein and tumor volume and increases survival. CD532 has been evaluated in animal models of N-Myc-driven cancers. In these studies, the compound is administered at various doses. Tumor volumes are measured. The compound drives MYCN degradation and exhibits anti-proliferative effects. The compound's ability to block Aurora A kinase activity contributes to its in vivo efficacy. |
| ADME/Pharmacokinetics |
No detailed pharmacokinetic data has been published for CD532. The compound has a molecular weight of 522.52 g/mol and a molecular formula of C26H25F3N8O. It has a purity of 98%. Further studies would be needed to characterize its absorption, distribution, metabolism, and excretion properties, including oral bioavailability, plasma protein binding, clearance, and half-life.
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| Toxicity/Toxicokinetics |
No detailed toxicity data has been published for CD532. As an Aurora A inhibitor, it may have on-target effects on mitosis in normal proliferating tissues. Comprehensive toxicology studies would be required to evaluate its safety profile for potential therapeutic development. The compound is intended for research use only.
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| References | |
| Additional Infomation |
CD532 belongs to the phenylurea class of compounds. Its structure is urea with 4-[[4-[(5-cyclopentylpyrazol-3-yl)amino]pyrimidin-2-yl]amino]phenyl and 3-[3-(trifluoromethyl)phenyl] substituents at the N1 and N3 positions, respectively. It is an antitumor drug. It is an aminopyrimidine compound, belonging to the secondary amino group, and is also a member of the pyrazole, cyclopentane, and phenylurea classes.
CD532 (CAS# 1639009-81-6) is a potent Aurora A kinase inhibitor with an IC50 of 45 nM. It breaks the native conformation of Aurora-A, drives N-Myc degradation in N-Myc-driven cancers, and exhibits anti-proliferative effects. CD532 (1-10000 nM; 72 h) is cytotoxic with EC50 values of 223.2 nM and 146.7 nM. It also inhibits several CDKs, FGFRs, MEKs, and PDGFRs. The molecular formula is C26H25F3N8O and molecular weight is 522.52 g/mol. The compound is used in cancer research. |
| Molecular Formula |
C26H25F3N8O
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|---|---|
| Molecular Weight |
522.524914503098
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| Exact Mass |
522.21
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| CAS # |
1639009-81-6
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| Related CAS # |
CD532 hydrochloride;2926498-81-7
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| PubChem CID |
77232197
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| Appearance |
White to off-white solid powder
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| LogP |
5.7
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| Hydrogen Bond Donor Count |
5
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| Hydrogen Bond Acceptor Count |
9
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| Rotatable Bond Count |
7
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| Heavy Atom Count |
38
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| Complexity |
759
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| Defined Atom Stereocenter Count |
0
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| SMILES |
FC(C1C=CC=C(C=1)NC(NC1C=CC(=CC=1)NC1=NC=CC(=N1)NC1C=C(C2CCCC2)NN=1)=O)(F)F
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| InChi Key |
GBMIFBVLJSCVJT-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C26H25F3N8O/c27-26(28,29)17-6-3-7-20(14-17)33-25(38)32-19-10-8-18(9-11-19)31-24-30-13-12-22(35-24)34-23-15-21(36-37-23)16-4-1-2-5-16/h3,6-16H,1-2,4-5H2,(H2,32,33,38)(H3,30,31,34,35,36,37)
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| Chemical Name |
1-[4-[[4-[(5-cyclopentyl-1H-pyrazol-3-yl)amino]pyrimidin-2-yl]amino]phenyl]-3-[3-(trifluoromethyl)phenyl]urea
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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 : 250 mg/mL (478.45 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (3.98 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 20.8 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: ≥ 2.08 mg/mL (3.98 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 20.8 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: ≥ 2.08 mg/mL (3.98 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.9138 mL | 9.5690 mL | 19.1380 mL | |
| 5 mM | 0.3828 mL | 1.9138 mL | 3.8276 mL | |
| 10 mM | 0.1914 mL | 0.9569 mL | 1.9138 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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