Nutrabiotech Alisertib MLN8237 98% 1G Powder, 98% high purity Alisertib MLN8237 powder, selective Aurora A kinase inhibitor, mitotic spindle regulator, G2/M cell cycle arrest anti-tumor research raw material

Alisertib MLN8237 CAS 1028486-01-2 High-Purity Powder Selective Aurora A Kinase Inhibitor Orally Bioavailable Anti-Tumor Biochemical Research Reagent

Premium Alisertib MLN8237 crystalline powder CAS 1028486-01-2, highly selective Aurora A kinase inhibitor lab-grade reagent. In stock for mitotic regulation and multi-type tumor pharmacology research.
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Alisertib (CAS 1028486-01-2) Aurora A Kinase Inhibitor | MLN8237, Selective Aurora A (AURKA) Inhibitor for Oncology

Alisertib CAS 1028486-01-2
Selective Aurora A Kinase Inhibitor (MLN8237)

Alisertib (CAS 1028486-01-2), also MLN8237, is a potent, orally bioavailable, ATP-competitive inhibitor highly selective for Aurora A kinase (IC50 ~1.2 nM) with >200-fold selectivity over Aurora B. It disrupts mitotic spindle assembly and chromosome alignment and, uniquely, disrupts the Aurora A/Myc complex to drive Myc degradation. Molecular formula C27H20ClFN4O4, MW 518.92. Research-grade with COA.

Aurora A Inhibitor AURKA MLN8237 Mitosis MYC Degradation Neuroblastoma SCLC Oncology
Request a Quote Technical Specs
518.92
MW (C27H20ClFN4O4)
1.2 nM
Aurora A IC50
>200x
vs Aurora B

Molecular Information

Name: Alisertib
CAS: 1028486-01-2
Formula: C27H20ClFN4O4
MW: 518.92 g/mol
Class: Benzazepine
Core: Pyrimido[5,4-d][2]benzazepine
Target: Aurora A kinase (AURKA)
IC50: 1.2 nM (AURKA)
Selectivity: >200x vs Aurora B
Appearance: White to khaki solid
Synonyms: MLN8237
Storage: -20 C
🧪
CAS Number
1028486-01-2
⚖️
Molecular Weight
518.92
🎯
Primary Activity
Aurora A Inhibitor
✅
Purity
≥98%

Product Technical Specifications

Complete physicochemical properties and QC parameters for Alisertib (CAS 1028486-01-2)

📋 Physicochemical Properties

  • Product NameAlisertib (MLN8237)
  • IUPAC Core4-[[9-chloro-7-(2-fluoro-6-methoxyphenyl)-5H-pyrimido[5,4-d][2]benzazepin-2-yl]amino]-2-methoxybenzoic acid
  • CAS Number1028486-01-2
  • SynonymsMLN8237; MLN 8237; MLN-8237
  • Molecular FormulaC27H20ClFN4O4
  • Molecular Weight518.92 g/mol
  • SourceSynthetic small molecule (Millennium/Takeda)
  • AppearanceWhite to khaki solid
  • Melting PointNot reported
  • Water SolubilityInsoluble
  • Organic SolubilityDMSO ~27 mg/mL; ethanol poorly
  • Compound ClassBenzazepine / Aurora A kinase inhibitor
  • HS Code2934.99

🔬 Quality Control & Handling

  • Purity (HPLC)≥98%
  • FormSolid powder
  • Primary TargetAurora A kinase (AURKA)
  • Pathway Readoutp-Histone H3 (Ser10) suppression; mitotic arrest; Myc loss
  • Selectivity>200-fold over Aurora B; minimal off-kinome activity
  • Storage Condition-20 C, sealed, protect from light
  • Solution StabilityAliquot DMSO stocks; avoid freeze-thaw
  • ShippingBlue ice / cold chain recommended
  • QC DocumentationCOA / HPLC / NMR / MS / MSDS
  • Pack Sizes1g / 5g / 10g / 100g / 1KG
  • Stock StatusIn Stock
  • Use StatementResearch use only; not for human/clinical use

Key Molecular Targets & Pathway Nodes

Alisertib's selectivity lets researchers isolate Aurora A biology from the overlapping but distinct Aurora B program that governs cytokinesis.

🧬 Aurora A (AURKA) 🧬 Aurora B (weak, >200x less) 🧩 TPX2 / Aurora A Complex 🧬 MYC / c-Myc 🧬 PLK1 / Mitotic Kinases 📈 p-Histone H3 (Ser10) 🔗 Centrosome & Spindle 🧬 Survivin / Chromosome Alignment 🧫 Neuroblastoma 🫁 Small Cell Lung Cancer 🧬 Lymphoma 🔬 Spindle-Assembly Checkpoint

How Alisertib Works: Poisoning the Mitotic Spindle

Alisertib occupies the Aurora A ATP pocket, collapsing spindle assembly and chromosome alignment

1

ATP-Pocket Blockade of Aurora A

Alisertib binds the ATP-binding pocket of Aurora A (AURKA) with ~1.2 nM potency and >200-fold selectivity over Aurora B. Because the two Aurora kinases drive distinct mitotic events, this selectivity enables clean dissection of Aurora A-specific phenotypes without the cytokinesis defects that dominate pan-Aurora drugs.

2

Spindle Assembly & Chromosome Alignment Failure

Aurora A phosphorylates substrates (e.g., with TPX2) that organize centrosomes and the mitotic spindle. Inhibition produces monopolar/spindle defects, misaligned chromosomes and a raised G2/M population, with loss of the mitotic marker phospho-Histone H3 (Ser10) — a canonical pharmacodynamic readout.

3

Disruption of Aurora A/Myc & Apoptosis

Uniquely among Aurora inhibitors, alisertib disrupts the Aurora A/Myc complex, driving Myc degradation — especially important in Myc-amplified neuroblastoma. Persistent mitotic stress triggers apoptosis, autophagy and multinucleation at higher concentrations, yielding broad anti-proliferative activity across tumor lines.

⚖️ Alisertib vs Other Aurora Inhibitors

  • Alisertib (this product)Selective Aurora A (IC50 1.2 nM); >200x vs B
  • Barasertib (AZD1152)Aurora B selective (Haspin-adjacent)
  • Tozasertib (VX-680)Pan-Aurora (A/B/C)
  • DanusertibPan-Aurora + off-target kinases
  • Selectivity EdgeClean Aurora A mechanistic studies
  • Unique FeatureDisrupts Aurora A/Myc complex (Myc degradation)

♻️ Downstream Biological Consequences

  • MitosisSpindle defects; chromosome misalignment
  • Cell CycleG2/M accumulation; mitotic arrest
  • Histone MarkReduced p-Histone H3 (Ser10)
  • OncoproteinMyc degradation (Aurora A/Myc disruption)
  • FateApoptosis & autophagy at higher dose
  • PhenotypeMultinucleation (Aurora B-like at high conc.)

Research Applications & Models

Aurora A is amplified in several cancers; alisertib's selectivity makes it both a therapeutic lead and a precise mitosis probe.

🧠

Neuroblastoma

A flagship alisertib indication: Aurora A is frequently amplified, and alisertib uniquely degrades Myc via Aurora A/Myc disruption, showing activity in MYC-driven and high-risk neuroblastoma models.

MYC / AURKA
🫁

Small Cell Lung Cancer (SCLC)

Studied with paclitaxel in SCLC where Aurora A is a mitotic vulnerability; clinically evaluated in Phase II combination approaches.

Mitotic Vulnerability
🧫

Mitotic Spindle Research

The definitive selective Aurora A tool for studying spindle assembly, centrosome maturation and chromosome alignment; benchmarked by p-Histone H3 (Ser10) loss and aligned-spindle assays.

Spindle / SAC
🧬

MYC-Driven Models

Used to probe Aurora A/Myc dependence and Myc-protein stability, a mechanism distinct from classical mitotic arrest — valuable in Myc-amplified cancers.

MYC Degradation
🩸

Lymphoma & Hematologic Malignancy

Shown to regress lymphoma xenografts; studied in diffuse large B-cell and other hematologic models where Aurora A supports proliferation.

Lymphoma
🧪

Kinase Selectivity Profiling

Its >200-fold Aurora A vs B selectivity makes it the comparator of choice when distinguishing Aurora A from Aurora B contributions in kinase panels.

Kinome Selectivity
🐭

In Vivo Efficacy & PD

Evaluated in subcutaneous and intracranial xenografts with p-Histone H3 as a PD biomarker; oral activity supports chronic dosing schedules.

Xenograft PD
🔬

Cell-Cycle Arrest Studies

Applied to map G2/M checkpoint engagement, apoptosis and autophagy induction across colon, lung, breast, prostate and ovarian lines.

Cell Cycle

Key Literature & Landmark Publications

Key references on alisertib pharmacology and Aurora A biology.

Manfredi MG, et al. Characterization of alisertib (MLN8237), an investigational small-molecule inhibitor of aurora A kinase using novel in vivo pharmacodynamic assays. Clin Cancer Res. 2011;17(24):7614-24.
doi: 10.1158/1078-0432.CCR-11-1464
Durlacher CT, et al. Alisertib: a highly selective Aurora A kinase inhibitor. Front Oncol. 2015;5:189.
doi: 10.3389/fonc.2015.00189
Brockmann M, et al. Aurora A kinase inhibition undermines MYCN- and MYC-driven cancers. Cancer Cell. 2013;24(1):75-89. (Aurora A/Myc).
doi: 10.1016/j.ccr.2013.05.011
Richards MW, et al. Structural basis of AURKA-TPX2-MYCN interactions and inhibition. (Aurora A/Myc complex).
Landmark reference
Dees EC, et al. Phase I study of aurora A kinase inhibitor MLN8237 in advanced solid tumors. Clin Cancer Res. 2012;18(16):4775-84. (clinical PK/PD).
Landmark reference

Available Sizes & Ordering

Research-grade Alisertib (CAS 1028486-01-2) with full QC documentation; standard packs and bulk custom quantities supported.

TierPack SizeStock StatusSuitable ForLead Time
Standard1gIn StockAurora A / mitotic cell assaysSame/next-day ship
Medium5gIn StockIn vivo tumor & spindle modelsSame/next-day ship
Large10gIn StockMYC-driven & combination studiesSame/next-day ship
Bulk100gIn StockFormulation & process developmentQuote to confirm
Industrial1KGMade to orderPilot/production scale, CMO supplyBatch delivery

💡 Reference sizes shown above; for exact pricing and availability please contact us for a quote. Bulk orders qualify for tiered discounts.

Frequently Asked Questions (FAQ)

What is alisertib and what is it selective for?
Alisertib (CAS 1028486-01-2), also MLN8237, is a potent, orally bioavailable, ATP-competitive inhibitor highly selective for Aurora A kinase (AURKA) (IC50 ~1.2 nM) with >200-fold selectivity over Aurora B. It is a benzazepine-class mitotic inhibitor. Formula C27H20ClFN4O4, MW 518.92.
What is the difference between Aurora A and Aurora B, and why does selectivity matter?
Both are mitotic serine/threonine kinases but govern different events: Aurora A organizes centrosomes and the spindle (with TPX2); Aurora B drives the spindle-assembly checkpoint and cytokinesis. Pan-Aurora drugs cause overlapping defects that obscure which kinase matters. Alisertib's >200-fold A-over-B selectivity lets researchers cleanly attribute phenotypes to Aurora A.
How does alisertib kill cancer cells?
It blocks Aurora A's ATP pocket, so spindle assembly and chromosome alignment fail — cells arrest in G2/M with loss of the mitotic marker phospho-Histone H3 (Ser10). Uniquely, alisertib also disrupts the Aurora A/Myc complex, driving Myc degradation (critical in MYC-amplified neuroblastoma). Persistent mitotic stress triggers apoptosis and autophagy.
Which tumors is alisertib studied in?
Most prominently neuroblastoma (Aurora A/MYC-driven), small-cell lung cancer (with taxanes), and lymphoma. It shows broad anti-proliferative activity across colon, lung, breast, prostate, ovarian and pancreatic lines and is a reference selective Aurora A agent in xenograft studies.
What is the aligned-spindles (AS) pharmacodynamic biomarker?
The aligned-spindles assay quantifies mitotic cells with correctly bipolar, aligned chromosomes; alisertib reduces this population by poisoning spindle assembly. It is a clinically validated PD biomarker used to confirm Aurora A target engagement in tumor tissue.
How soluble is alisertib and how should it be prepared?
Alisertib is soluble in DMSO (~27 mg/mL) but insoluble in water and poorly in ethanol. For cell assays dilute the DMSO stock into medium (final DMSO ≤0.1% v/v); active concentrations are typically low nanomolar to low micromolar. Store solid at -20 C and aliquot stocks to avoid freeze-thaw.
Is QC documentation provided?
Every batch ships with a Certificate of Analysis (COA) including HPLC purity, NMR structural confirmation and MS data. MSDS/SDS, residual-solvent data and Certificates of Origin are available on request. Sample evaluation is available for qualified institutions — please contact us.

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Research-grade Alisertib (CAS 1028486-01-2) — purity ≥98% HPLC, COA included
MLN8237 — >200-fold selective Aurora A kinase inhibitor that disrupts mitosis and degrades Myc — request a quote today

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Weight 1 g

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