We use analytics and advertising cookies, which you can accept or reject; see our privacy policy.

Current choice:

Fig. 1 · Structure
Cat. No.
A10184
CAS No.
942947-93-5
Formula
C23H25ClN8OS
Mol. Weight
497

Documents & Downloads

CCT129202

Cat. No. A10184 CAS 942947-93-5

Aurora Inhibitor

CCT129202 is a representative of a structurally novel series of imidazopyridine small-molecule inhibitors of Aurora kinase activity. It shows high selectivity for the Aurora kinases over a panel of other kinases tested and inhibits proliferation in multiple cultured human tumor cell lines.

In Stock

Notify me when the price drops

For laboratory research use only. We do not sell to patients.

Free Aliquoting for Your Order

Tell us your preferred amount per vial. We’ll confirm the options.

Biological Activity

Bioactivity / Mechanism

CCT129202 showed cellular activity consistent with Aurora-kinase inhibition in C1 and KOPN8 B-ALL cells. Treatment at 1 μM for 18 hours reduced phospho-Aurora immunoblot signal and was accompanied by PARP and caspase-7 cleavage relative to vehicle controls. These qualitative cellular readouts do not establish isoform-selective biochemical potency. [1]

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

Target & Activity

Target Activity Value
Aurora A 42 nM
Aurora B 198 nM
Aurora C 227 nM

Cellular Effect

Cell Line Activity Value Description Reference
HCT-116 GI50 0.35 μM Growth inhibition of human HCT116 cells after 72 hrs by MTT assay [PMID: 20565112]

In Vitro Studies

CCT129202 responses varied across a 14-line leukemia panel after four days of exposure. Reported cellular IC50 values included 0.05±0.005 μM in TIB-202 and 0.1±0.06 μM in MV4-11, while NB4 had IC50 >10 μM. Normal lymphocytes also had IC50 >10 μM, but bone marrow stroma had IC50 1±0.7 μM. Values with ± are reported with standard deviations; the table describes three separate experiments. The overlapping responses limit broad claims of cancer-cell selectivity. [1]

Variable cellular sensitivity across a leukemia panel and normal-cell comparators

Cell-based study · Fourteen human leukemia cell lines, normal lymphocytes and bone marrow stroma. [1]

Four-day cytotoxicity profiling showed heterogeneous responses. TIB-202 and MV4-11 were sensitive, while NB4 did not reach the reported IC50 within the tested range. Normal lymphocytes had IC50 >10 μM, but bone marrow stroma had IC50 1±0.7 μM, overlapping several leukemia lines. Values are reported cellular assay IC50s, not kinase inhibition constants or treatment recommendations.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
C1 cellular viability/growth inhibition relative to DMSO controlCellular IC50 3±0.8 μM[1]
SEM cellular viability/growth inhibition relative to DMSO controlCellular IC50 0.8±0.3 μM[1]
B1 cellular viability/growth inhibition relative to DMSO controlCellular IC50 3±0.6 μM[1]
UOCB1 cellular viability/growth inhibition relative to DMSO controlCellular IC50 0.9±0.09 μM[1]
Nalm6 cellular viability/growth inhibition relative to DMSO controlCellular IC50 2±0.8 μM[1]
KOPN8 cellular viability/growth inhibition relative to DMSO controlCellular IC50 0.7±0.1 μM[1]
CEM cellular viability/growth inhibition relative to DMSO controlCellular IC50 0.9±0.05 μM[1]
Molt-3 cellular viability/growth inhibition relative to DMSO controlCellular IC50 2±0.6 μM[1]
Molm13 cellular viability/growth inhibition relative to DMSO controlCellular IC50 5±0.9 μM[1]
MV4-11 cellular viability/growth inhibition relative to DMSO controlCellular IC50 0.1±0.06 μM[1]
TIB-202 cellular viability/growth inhibition relative to DMSO controlCellular IC50 0.05±0.005 μM[1]
NB4 cellular viability/growth inhibition relative to DMSO controlCellular IC50 >10 μM[1]
HL-60 cellular viability/growth inhibition relative to DMSO controlCellular IC50 7±0.8 μM[1]
HL-60 RA cellular viability/growth inhibition relative to DMSO controlCellular IC50 8±0.5 μM[1]
Normal lymphocytes cellular viability/growth inhibition relative to DMSO controlCellular IC50 >10 μM[1]
Bone marrow stroma cellular viability/growth inhibition relative to DMSO controlCellular IC50 1±0.7 μM[1]

Literature-Reported Treatment Conditions

Treatment concentration
Eight tested concentrations spanning 1×10^-6 to 10 μM (Table 2 caption); individual intermediate concentrations not listed there.
Exposure duration
4 days before viability assessment; Alamar blue incubation, when used, lasted up to 24 hours.
Method
Single-agent concentration-response profiling; Alamar blue assay or automated microscopy, normalized to DMSO-treated cells.
Vehicle
DMSO; final percentage not specified for this assay in the read methods.
Reported limits
Table 2 does not assign the viability method to each individual cell-line entry. Salt/solvate and compound lot are not specified.
Methods and source locations

Compound reported in the paper: CCT129202; Compound label in the paper: CCT129202

Evidence concerns the named research compound; it does not validate an Adooq lot or establish interchangeability of formulations.

Table 2, CCT129202 rows and caption; Materials and Methods: Aurora Kinase Inhibitors and Cytotoxicity Assays

C1 cellular viability/growth inhibition relative to DMSO control: Four-day exposure; Alamar blue or automated microscopy. ± denotes SD; caption describes three separate experiments. — Table 2, CCT129202 row, C1 column and caption

SEM cellular viability/growth inhibition relative to DMSO control: Four-day exposure; Alamar blue or automated microscopy. ± denotes SD; caption describes three separate experiments. — Table 2, CCT129202 row, SEM column and caption

B1 cellular viability/growth inhibition relative to DMSO control: Four-day exposure; Alamar blue or automated microscopy. ± denotes SD; caption describes three separate experiments. — Table 2, CCT129202 row, B1 column and caption

UOCB1 cellular viability/growth inhibition relative to DMSO control: Four-day exposure; Alamar blue or automated microscopy. ± denotes SD; caption describes three separate experiments. — Table 2, CCT129202 row, UOCB1 column and caption

Nalm6 cellular viability/growth inhibition relative to DMSO control: Four-day exposure; Alamar blue or automated microscopy. ± denotes SD; caption describes three separate experiments. — Table 2, CCT129202 row, Nalm6 column and caption

KOPN8 cellular viability/growth inhibition relative to DMSO control: Four-day exposure; Alamar blue or automated microscopy. ± denotes SD; caption describes three separate experiments. — Table 2, CCT129202 row, KOPN8 column and caption

CEM cellular viability/growth inhibition relative to DMSO control: Four-day exposure; Alamar blue or automated microscopy. ± denotes SD; caption describes three separate experiments. — Table 2, CCT129202 row, CEM column and caption

Molt-3 cellular viability/growth inhibition relative to DMSO control: Four-day exposure; Alamar blue or automated microscopy. ± denotes SD; caption describes three separate experiments. — Table 2, CCT129202 row, Molt-3 column and caption

Molm13 cellular viability/growth inhibition relative to DMSO control: Four-day exposure; Alamar blue or automated microscopy. ± denotes SD; caption describes three separate experiments. — Table 2, CCT129202 row, Molm13 column and caption

MV4-11 cellular viability/growth inhibition relative to DMSO control: Four-day exposure; Alamar blue or automated microscopy. ± denotes SD; caption describes three separate experiments. — Table 2, CCT129202 row, MV4-11 column and caption

TIB-202 cellular viability/growth inhibition relative to DMSO control: Four-day exposure; Alamar blue or automated microscopy. ± denotes SD; caption describes three separate experiments. — Table 2, CCT129202 row, TIB-202 column and caption

NB4 cellular viability/growth inhibition relative to DMSO control: Four-day exposure; Alamar blue or automated microscopy. ± denotes SD; caption describes three separate experiments. — Table 2, CCT129202 row, NB4 column and caption

HL-60 cellular viability/growth inhibition relative to DMSO control: Four-day exposure; Alamar blue or automated microscopy. ± denotes SD; caption describes three separate experiments. — Table 2, CCT129202 row, HL-60 column and caption

HL-60 RA cellular viability/growth inhibition relative to DMSO control: Four-day exposure; Alamar blue or automated microscopy. ± denotes SD; caption describes three separate experiments. — Table 2, CCT129202 row, HL-60 RA column and caption

Normal lymphocytes cellular viability/growth inhibition relative to DMSO control: Four-day exposure; Alamar blue or automated microscopy. ± denotes SD; caption describes three separate experiments. — Table 2, CCT129202 row, Normal lymphocytes column and caption

Bone marrow stroma cellular viability/growth inhibition relative to DMSO control: Four-day exposure; Alamar blue or automated microscopy. ± denotes SD; caption describes three separate experiments. — Table 2, CCT129202 row, Bone marrow stroma column and caption

Aurora phosphorylation and apoptotic-marker responses in B-ALL cells

Cell-based study · Human B-ALL cell lines C1 and KOPN8. [1]

At 1 μM for 18 hours, CCT129202-treated cells showed reduced phospho-Aurora signal and cleavage of PARP and caspase 7 relative to the matching DMSO1 lanes. These qualitative immunoblot findings support cellular Aurora-pathway modulation with apoptotic-marker processing; they do not quantify isoform-selective potency or prove that every cellular effect is Aurora-dependent.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Phospho-Aurora A/B/C immunoblot signal and PARP/caspase-7 cleavage in C1 and KOPN8Qualitative immunoblot response Reduced phospho-Aurora signal with PARP and caspase-7 cleavage relative to DMSO1; representative of three separate experiments.[1]

Literature-Reported Treatment Conditions

Treatment concentration
1 μM
Exposure duration
18 hours
Method
Single-agent treatment followed by immunoblot analysis of cellular extracts.
Vehicle
DMSO; DMSO1 is the control for the first inhibitor group containing CCT129202.
Reported limits
Final DMSO percentage and quantitative densitometry are not specified in the read experiment description. No isoform-specific IC50 can be inferred.
Methods and source locations

Compound reported in the paper: CCT129202; Compound label in the paper: CCT lane in Figure 3

Evidence concerns the named research compound; it does not validate an Adooq lot or establish interchangeability of formulations.

Figure 3 and caption; Results: Aurora Kinase Inhibition By Targeted Therapeutics Promotes Changes In Aurora Kinase Activity And The Induction Of Apoptosis; Methods: Aurora Kinase Inhibitors, Preparation Of Cellular Extracts and Immunoblotting

Phospho-Aurora A/B/C immunoblot signal and PARP/caspase-7 cleavage in C1 and KOPN8: Immunoblotting; total Aurora A/B and β-actin monitored. No densitometric percentage extracted. — Figure 3, CCT and DMSO1 lanes in both cell lines; caption; Results: Aurora Kinase Inhibition By Targeted Therapeutics Promotes Changes In Aurora Kinase Activity And The Induction Of Apoptosis

In Vivo Studies

A larval zebrafish screen found a dramatically reduced retinal ciliary marginal-zone proliferative region after CCT129202 exposure at 20 μM for four days. This was a qualitative finding based on one representative CMZ image from one individual per treatment group. It provides a developmental-model limitation on interpreting the compound’s effects and does not establish mammalian efficacy or a safety threshold. [2]

Qualitative reduction of the retinal ciliary marginal zone in larval zebrafish

Animal study · Larval Tg(hsp70:HA-mCherryTM) zebrafish with GFP-labeled rods; retinal ciliary marginal zone. [2]

In a single-concentration screen, the representative CCT129202-treated retinal image showed a dramatically reduced proliferative zone at the ciliary margin compared with the DMSO control. This is a developmental retinal phenotype at 20 μM exposure, not a mammalian antitumor efficacy or safety study. CMZ assessment used one representative image from one individual per treatment group.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Morphology of the proliferative zone at the retinal ciliary marginal zoneQualitative confocal-image assessment Dramatically reduced proliferative zone in the representative CCT129202 image; no numerical effect size or statistical test assigned to this CMZ observation.[2]

Conditions shared by the study groups

Route
Waterborne exposure
Frequency
Continuous exposure; water/compound not exchanged during the four-day period.
Treatment course
4 days
Vehicle
DMSO-based library stock; 0.2% DMSO vehicle comparator.
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
CCT129202 retinal-screen arm
20 μM nominal concentration in exposure water; not a mg/kg dose.		DMSO-treated larvae; Figure 6c.Representative CCT129202 image in Figure 6f shows dramatic reduction of the CMZ proliferative zone. The CMZ image is from one individual, not a replicated quantitative cohort endpoint.[2]
CCT129202 retinal-screen arm
Model: Larval zebrafish retina, 6–10 days post-fertilization.
Reported limits: Salt/solvate and internal tissue concentration not established; CMZ result does not provide a numerical safety threshold.
Methods and source locations

Compound reported in the paper: CCT129202; Compound label in the paper: CCT129202 in Figure 6f

Qualitative larval zebrafish finding for the named compound under a single screening exposure; no Adooq-lot or mammalian safety validation.

Figure 6c/f and caption; Results: ciliary marginal zone; Methods: Heat shock and compound treatment and Image collection and analysis; Discussion: low-n CMZ limitation

Morphology of the proliferative zone at the retinal ciliary marginal zone: Retinal immunofluorescence and confocal imaging; one representative CMZ image from one individual in each treatment group. — Figure 6c and 6f (CCT129202 panel) and caption; Results: ciliary marginal zone; Materials and Methods: Image collection and analysis

CCT129202 retinal-screen arm · Figure 6c/f and caption; Methods: Heat shock and compound treatment and Image collection and analysis

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 942947-93-5
Applications Aurora Inhibitor
Formula C23H25ClN8OS
Molecular Weight 497
SMILES
CN(C)C1=CC=C(C=C1)C2=NC3=NC=C(C(=C3N2)N4CCN(CC4)CC(=O)NC5=NC=CS5)Cl

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 3 mg/mL (6.03 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
28 mg/mL
Vehicle
1% DMSO+30% polyethylene glycol+1% Tween 80

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] Jayanthan A, Ruan Y, Truong TH, et al. Aurora kinases as druggable targets in pediatric leukemia: heterogeneity in target modulation activities and cytotoxicity by diverse novel therapeutic agents PloS one (2014). PMID: 25048812 DOI: 10.1371/journal.pone.0102741 Source material
  2. [2] Campbell LJ, West MC, Jensen AM. A high content, small molecule screen identifies candidate molecular pathways that regulate rod photoreceptor outer segment renewal Scientific reports (2018). PMID: 30228302 DOI: 10.1038/s41598-018-32336-y Source material

Added to your cart

View Cart Checkout
Loading...