2. Cell Cycle/DNA Damage Epigenetics Protein Tyrosine Kinase/RTK Metabolic Enzyme/Protease Apoptosis NF-κB Immunology/Inflammation
  3. Aurora Kinase Anaplastic lymphoma kinase (ALK) Mitochondrial Metabolism Apoptosis Reactive Oxygen Species (ROS) Aldehyde Dehydrogenase (ALDH)
  4. Aurora kinase/ALK-IN-1

Aurora kinase/ALK-IN-1 is a dual Aurora A kinase and ALK inhibitor with IC50 values of 0.296 μM and 0.332 μM, respectively. Aurora kinase/ALK-IN-1 induces G2/M cell cycle arrest, triggers mitochondrial apoptosis, elevates intracellular reactive oxygen species (ROS) levels, and inhibits ALDH1 activity. Aurora kinase/ALK-IN-1 demonstrates cytotoxicity and tumor selectivity. Aurora kinase/ALK-IN-1 can be used for the research of anaplastic large cell lymphoma.

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Aurora kinase/ALK-IN-1

Aurora kinase/ALK-IN-1 Chemical Structure

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Aurora kinase/ALK-IN-1 Related Antibodies

Top Publications Citing Use of Products

View All Aurora Kinase Isoform Specific Products:

View All Isoforms
Aurora Kinase Aurora A Aurora B Aurora C

View All Aldehyde Dehydrogenase (ALDH) Isoform Specific Products:

View All Isoforms
ALDH1 ALDH2 ALDH3

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Description

Aurora kinase/ALK-IN-1 is a dual Aurora A kinase and ALK inhibitor with IC50 values of 0.296 μM and 0.332 μM, respectively. Aurora kinase/ALK-IN-1 induces G2/M cell cycle arrest, triggers mitochondrial apoptosis, elevates intracellular reactive oxygen species (ROS) levels, and inhibits ALDH1 activity. Aurora kinase/ALK-IN-1 demonstrates cytotoxicity and tumor selectivity. Aurora kinase/ALK-IN-1 can be used for the research of anaplastic large cell lymphoma[1].

IC50 & Target[1]

Aurora A

0.296 μM (IC50)

Aurora B

0.887 μM (IC50)

In Vitro

Aurora kinase/ALK-IN-1 (compound 22h) (48 h) exhibits potent, selective cytotoxicity against ALK+ ALCL SR cells with an IC50 of 5.10 μM, showing a 7-fold selectivity margin over normal human peripheral blood mononuclear cells[1].
Aurora kinase/ALK-IN-1 (5-10 μM; 24 h) induces dose-dependent depletion of phosphorylated and total Aurora A and ALK in ALK+ ALCL SR cells[1].
Aurora kinase/ALK-IN-1 (5-10 μM; 24 h) induces dose-dependent G2/M cell cycle arrest in ALK+ ALCL SR cells[1].
Aurora kinase/ALK-IN-1 (5-10 μM; 48 h) induces dose-dependent mitochondrial apoptosis in ALK+ ALCL SR cells[1].
Aurora kinase/ALK-IN-1 (5-10 μM; 24 h) elevates intracellular ROS levels in ALK+ ALCL SR cells to 3.5-fold above control levels after 24 h of treatment[1].
Aurora kinase/ALK-IN-1 (24 h) inhibits ALDH1 enzyme activity in ALK+ ALCL SR cell lysates with an IC50 of 2.8 μg/mL, reducing activity by 2.8-fold at 10 μM[1].
Aurora kinase/ALK-IN-1 (5-10 μM; 48 h) synergistically potentiates Ara-C cytotoxicity in ALK+ ALCL SR cells[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Aurora kinase/ALK-IN-1 Related Antibodies

Western Blot Analysis[1]

Cell Line: ALK+ ALCL SR cells
Concentration: 5; 10 μM
Incubation Time: 24 h
Result: Induced a dose-dependent reduction in both phosphorylated and total levels of Aurora A and ALK.
Maintained the ratio of phosphorylated to total protein constant relative to vehicle controls.

Cell Cycle Analysis[1]

Cell Line: ALK+ ALCL SR cells
Concentration: 5; 10 μM
Incubation Time: 24 h
Result: Induced a dose-dependent accumulation of cells in the G2/M phase.
Caused a 2.4-fold increase at 5 μM relative to vehicle controls.
Caused a 3.2-fold increase at 10 μM relative to vehicle controls.
Accompanied by reductions in G1 and S phase populations.

Apoptosis Analysis[1]

Cell Line: ALK+ ALCL SR cells
Concentration: 5; 10 μM
Incubation Time: 48 h
Result: Induced a dose-dependent increase in total apoptotic cells.
Resulted in 8.1% total apoptosis at 5 μM relative to ~0.2% in vehicle controls.
Resulted in 17.8% total apoptosis at 10 μM relative to ~0.2% in vehicle controls.

ELISA Assay[1]

Cell Line: ALK+ ALCL SR cells
Concentration: 5; 10 μM
Incubation Time: 24 h
Result: Induced a marked increase in intracellular ROS, reaching 3.5-fold above vehicle control values.

Cell Cytotoxicity Assay[1]

Cell Line: ALK+ ALCL SR cells, normal human peripheral blood mononuclear cells PCS-800-017
Concentration: 5; 10 μM
Incubation Time: 48 h
Result: Co-treatment with 10 μM Aurora kinase/ALK-IN-1 reduced the Ara-C IC50 in SR cells from 27.65 μM to 2.15 μM (12.8-fold increase in potency).
Had a Combination Index (CI) of 0.78 indicating synergy.
The combination yielded a selectivity index (SI) of 29.6, representing a 14.1-fold improvement in selectivity over Ara-C alone.
Molecular Weight

484.64

Formula

C17H20N6O3S4
SMILES

S=C(SC(SC(N(C)C)=S)C(C1=C(C)N(C2=CC=C([N+]([O-])=O)C=C2)N=N1)=O)N(C)C
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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Aurora kinase/ALK-IN-1 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Aurora kinase/ALK-IN-1Aurora KinaseAnaplastic lymphoma kinase (ALK)Mitochondrial MetabolismApoptosisReactive Oxygen Species (ROS)Aldehyde Dehydrogenase (ALDH)Anaplastic lymphoma kinaseALK tyrosine kinase receptorCD246Cluster of differentiation 246anaplastic large cell lymphomaperipheral blood mononuclear cellscytarabineAurora A kinaseALDH1mitochondrial apoptosisreactive oxygen speciesG2/M cell cycle arrestCys290anaplastic lymphoma kinaseInhibitorinhibitorinhibit

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