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Fig. 1 · Structure
Cat. No.
A11067
CAS No.
934541-31-8
Formula
C28H32N4O3S
Mol. Weight
504.6

Documents & Downloads

TAK-901

Cat. No. A11067 CAS 934541-31-8

Aurora Kinase A/B inhibitor

TAK-901 is a novel inhibitor of Aurora A/B with IC50 of 21 nM/15 nM. It is not a potent inhibitor of cellular JAK2, c-Src or Abl. Phase 1.

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Biological Activity

Target & Activity

Target Activity Value
JAK3 IC50 1.2nM
c-Src IC50 1.3nM
CLK2 IC50 <2.0nM
FGR IC50 <2.0nM
YES1 IC50 <2.0nM
LRRK2 IC50 3.0nM
FLT3 IC50 5.0nM
Fyn IC50 5.3nM
ARG IC50 5.6nM
Axl IC50 5.8nM
Hck IC50 5.8nM
SNF1LK2 IC50 6.0nM
Abl IC50 6.4nM
RET IC50 6.5nM
TrkA IC50 6.7nM
LCK IC50 6.8nM
PTK5 IC50 7.1nM
Fms IC50 7.2nM
FGFR2 IC50 7.3nM
EphB1 IC50 8.9nM
Abl(T315I) IC50 9.0nM
EphA1 IC50 9.1nM
ARK5 IC50 9.1nM
ITK IC50 12nM
ALK2 IC50 13nM
CDK7 IC50 14nM
BLK IC50 14nM
AuroraB-INCENP IC50 15nM
JAK2 IC50 17nM
EphB2 IC50 18nM
AuroraA-TPX2 IC50 21nM
STK16 IC50 24nM
EphA2 IC50 24nM
BRK IC50 25nM
EphB4 IC50 27nM
TNK2 IC50 27nM
FGFR1 IC50 28nM
EphA4 IC50 31nM
STK33 IC50 35nM
CLK1 IC50 45nM
AMPK IC50 46nM
FES IC50 48nM
SLK IC50 49nM
Chk2 IC50 50nM
TYK2 IC50 54nM
BTK IC50 55nM
FAK2 IC50 55nM
c-Kit IC50 58nM
VEGFR2 IC50 60nM
FGFR3 IC50 65nM
ALK5 IC50 78nM
MAP3K9 IC50 80nM
CLK3 IC50 88nM
JAK1 IC50 93nM

54 targets · Scroll to view more

In Vitro Studies

In MDA-MB-231 cells treated with TAK-901, RNA-seq analysis showed similar trends to those observed with ENMD-2076. TAK-901-treated TNBC1 organoids had a lower viable cell percentage than the DMSO control. In U87MG cells treated with TAK-901 or vehicle, RT-qPCR validated inhibition of identified lipid metabolism genes. [1,2,3]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

RNA sequencing trends in MDA-MB-231 cells

Cell-based study · MDA-MB-231 cells [1]

MDA-MB-231 cells were treated with TAK-901 at 1 or 2 μM for 24 hours, with DMSO as the control. RNA-seq analysis showed similar trends to those observed with ENMD-2076.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
GSEA of RNA-seq resultsReported result TAK-901 at 1 or 2 μM for 24 hours: RNA-seq analysis showed similar trends as with ENMD-2076.[1]

Literature-Reported Treatment Conditions

Treatment concentration
1 or 2 μM
Exposure duration
for 24 hours
Vehicle
DMSO
Reported limits
Not stated in the sentences used: route.
Methods and source locations

Compound reported in the paper: TAK-901

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

RESULTS > HTS2 screening identified aurora kinase inhibitors that reprogram the expression of TIP signature genes in TNBC cells (S42); MATERIALS AND METHODS > RNA sequencing (S145); MATERIALS AND METHODS > Gene Ontology and GSEA (S153); MATERIALS AND METHODS > Chemicals (S167); Fig. 4 legend (S221)

GSEA of RNA-seq results: GSEA of RNA-seq results; comparator: dimethyl sulfoxide (DMSO) — RESULTS > HTS2 screening identified aurora kinase inhibitors that reprogram the expression of TIP signature genes in TNBC cells (S42); MATERIALS AND METHODS > RNA sequencing (S145); Fig. 4 legend (S221)

Organoid viability following compound treatment

Cell-based study · TNBC1 organoids [2]

In TNBC1 organoids, the tested compound at 10 µM yielded a viable cell percentage of 23.22 ± 9.64%, compared with 97.38 ± 5.86% for DMSO (p < 0.001).

Measured endpoints — not treatment concentrations
EndpointReported resultReference
viable cell percentageviable cell percentage TNBC1, 5-day exposure to 10 µM: 23.22 ± 9.64%[2]

Literature-Reported Treatment Conditions

Treatment concentration
10 µM
Exposure duration
administered two days post-passage of the organoids, and their effects were evaluated after five days
Co-treatment
Other interventions in this design: P/S 1×; HEPES 1×; B27 1×; Promicin 1×; N-acetylcysteine 1.25 μM; Rspo1 250 ng/mL; Noggin 100 ng/mL; EGF 5 ng/mL; A83-01 0.5 μM; SB202190 500 nM; Neuregulin 1 5 nM; FGF7 5 ng/mL; FGF10 20 ng/mL; Y27632 5 μM. Compound effect isolated by the comparison: vs. control.
Reported limits
Not stated in the sentences used: route, vehicle.
Methods and source locations

Compound reported in the paper: TAK-901

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

2. Results > 2.2. Growth Inhibition Profiling of Epigenetic Drugs on TNBC Organoids and Cell Lines (S21); 2. Results > 2.4. Superior Cytotoxicity of Novel Agents Panobinostat, Pacritinib, TAK-901, and JIB-04 over Paclitaxel in TNBC Organoid Models (S43, S44, S48, S49); 4. Materials and Methods > 4.2. Tissue Processing and Organoid Culture (S69); Figure 4 legend (S135, S137)

viable cell percentage: viable cell percentage; comparator: DMSO — 2. Results > 2.4. Superior Cytotoxicity of Novel Agents Panobinostat, Pacritinib, TAK-901, and JIB-04 over Paclitaxel in TNBC Organoid Models (S49); Figure 4 legend (S137)

Lipid metabolism gene expression in U87MG cells

Cell-based study · U87MG cells [3]

U87MG cells were treated with TAK-901 at 10 μM or vehicle for 72 h. RT-qPCR validated inhibition of identified lipid metabolism genes, including SREBF1, ACLY, ASCC2, FASN, SCD, and FADS1.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Expression of genes related to fatty acid metabolismReported result U87MG cells were treated with 10 μM TAK901 or vehicle for 72 h. The inhibition of some identified lipid metabolism genes were validated using RT-qPCR assays, including SREBF1, ACLY, ASCC2, FASN, SCD, and FADS1.[3]

Literature-Reported Treatment Conditions

Treatment concentration
10 μM
Exposure duration
72 h
Reported limits
Not stated in the sentences used: route, vehicle.
Methods and source locations

Compound reported in the paper: TAK-901

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

3. Results > 3.4. TAK901 Reduces the Expression of Genes Involved in Lipid Metabolism (S129); Figure 4 legend (S218, S220)

Expression of genes related to fatty acid metabolism: Expression of genes related to fatty acid metabolism; comparator: vehicle — 3. Results > 3.4. TAK901 Reduces the Expression of Genes Involved in Lipid Metabolism (S129); Figure 4 legend (S218, S220)

In Vivo Studies

Female BALB/c nude mice received TAK-901 by stereotaxic injection twice weekly, with vehicle as the control. Tumor size and the proliferation marker Ki67 were reduced in the TAK-901-treated group. [3]

Tumor size and Ki67 in BALB/c nude mice

Animal study · 6–8 week-old female BALB/c nude mice [3]

Female BALB/c nude mice received TAK-901 by stereotaxic injection twice weekly, with vehicle as the control. Tumor size and the proliferation marker Ki67 were reduced in the TAK-901-treated group.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
The tumor volume was quantified based on the H&E pictures.Reported result 5 μL of 2 mM TAK901; injection frequency was twice weekly: both tumor size and proliferation marker Ki67 were reduced in the TAK901-treated group.[3]

Conditions shared by the study groups

Route
stereotaxic injection
Treatment course
After 7 days; the injection frequency was twice weekly. Mice were sacrificed on day 17.
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
TAK-901 5 μL of 2 mMvehicle5 μL of 2 mM TAK901; injection frequency was twice weekly: both tumor size and proliferation marker Ki67 were reduced in the TAK901-treated group.[3]
TAK-901 5 μL of 2 mM
Model: 6–8 week-old female BALB/c nude mice
Reported limits: Not stated in the sentences used: vehicle.
Methods and source locations

Compound reported in the paper: TAK-901

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

2. Materials and Methods > 2.15. In Vivo Orthotopic Tumor Mouse Model (S74, S77, S78); 3. Results > 3.3. TAK901 Inhibits GBM Growth in Orthotopic Xenograft Mouse Models (S116, S118); Figure 3 legend (S191, S193)

The tumor volume was quantified based on the H&E pictures.: The tumor volume was quantified based on the H&E pictures.; comparator: vehicle — 2. Materials and Methods > 2.15. In Vivo Orthotopic Tumor Mouse Model (S77, S78); 3. Results > 3.3. TAK901 Inhibits GBM Growth in Orthotopic Xenograft Mouse Models (S118); Figure 3 legend (S193)

TAK-901 5 μL of 2 mM · 2. Materials and Methods > 2.15. In Vivo Orthotopic Tumor Mouse Model (S77, S78); 3. Results > 3.3. TAK901 Inhibits GBM Growth in Orthotopic Xenograft Mouse Models (S118); Figure 3 legend (S191)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 934541-31-8
Applications Aurora Kinase A/B inhibitor
Formula C28H32N4O3S
Molecular Weight 504.6
SMILES
CCS(=O)(=O)C1=CC=CC(=C1)C2=CC(=C(C3=C2C4=CC(=CN=C4N3)C)C)C(=O)NC5CCN(CC5)C

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 95 mg/mL (188.25 mM)
Water Insoluble
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration
4 mg/mL
Vehicle
2% DMSO +30% PEG 300+2% Tween 80+ddH2O

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Wang H, Li S, Wang Q, et al. Tumor immunological phenotype signature-based high-throughput screening for the discovery of combination immunotherapy compounds. Sci Adv (2021). PMID: 33523948 DOI: 10.1126/sciadv.abd7851 Source material
  2. [2] Rao X, Qiao Z, Yang Y, et al. Unveiling Epigenetic Vulnerabilities in Triple-Negative Breast Cancer through 3D Organoid Drug Screening. Pharmaceuticals (Basel) (2024). PMID: 38399440 DOI: 10.3390/ph17020225 Source material
  3. [3] Zhan X, Qiu R, He Y, et al. The Aurora Kinase Inhibitor TAK901 Inhibits Glioblastoma Growth by Blocking SREBP1-Mediated Lipid Metabolism. Cancers (Basel) (2022). PMID: 36497287 DOI: 10.3390/cancers14235805 Source material

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