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Fig. 1 · Structure
Cat. No.
A10714
CAS No.
398493-79-3
Formula
C28H35N7O2
Mol. Weight
501.6

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PHA-680632

Cat. No. A10714 CAS 398493-79-3

Aurora inhibitor

PHA-680632 is potent inhibitor of Aurora A, Aurora B and Aurora C with IC50 of 27 nM, 135 nM and 120 nM, respectively. It has 10- to 200-fold higher IC50 for FGFR1, FLT3, LCK, PLK1, STLK2, and VEGFR2/3.

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Biological Activity

Target & Activity

Target Activity Value
AuroraA IC50 27nM
AuroraC IC50 120nM
AuroraB IC50 135nM
FGFR1 IC50 390nM
PLK1 IC50 780nM
FLT3 IC50 820nM
VEGFR3 IC50 1000nM
VEGFR2 IC50 1920nM
LCK IC50 1950nM
STLK2 IC50 5500nM

10 targets · Scroll to view more

Cellular Effect

Cell Line Activity Value Description Reference
HCT-116 IC50 0.045 μM Antiproliferative activity against human HCT116 cells assessed as BrdU incorporation after 72 hrs [PMID: 19320489]
MOLT-4 EC50 0.22 μM Cytotoxicity against human MOLT4 cells assessed as inhibition of cell growth after 4 days by Cell Titer Blue end-point assay [PMID: 22889561]

In Vitro Studies

PHA-680632 was evaluated in neuroblastoma cells exposed to KCl. Compared with KCl alone, PHA-680632 completely abolished the KCl-induced increase in exon-6-3′UTR long luciferase activity. [1]

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

Suppression of KCl-induced luciferase activity in neuroblastoma cells

Cell-based study · Neuroblastoma cells [1]

Neuroblastoma cells underwent 20 mM KCl treatment for 3 h and PHA-680632 treatment for 30 min. Compared with KCl alone, PHA-680632 completely abolished the KCl-induced almost 300% increase in exon-6-3′UTR long luciferase activity.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
exon-6-3′UTR long luciferase activityReported result High KCl induced an almost 300% increase in exon-6-3′UTR long luciferase activity; completely abolished by PHA-680632 aurora-kinases inhibitor (P=0.796 one-way ANOVA; Fig. 4F)[1]

Literature-Reported Treatment Conditions

Exposure duration
20 mM KCl treatment for 3 h; PHA-680632 (aurora inhibitor) for 30 min of treatment
Co-treatment
Other interventions in this design: KCl 20 mM; 9-cis retinoic acid 5 µM. Compound effect isolated by the comparison: KCl 20 mM alone or in the presence of PHA-680632.
Reported limits
Not stated in the sentences used: dose, route, vehicle.
Methods and source locations

Compound reported in the paper: PHA-680632

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

RESULTS > Effects of aurora kinases inhibition on BDNF protein production (S88, S95, S96); MATERIALS AND METHODS > Cell cultures and reagents (S100); MATERIALS AND METHODS > Luciferase assay (S129, S131)

exon-6-3′UTR long luciferase activity: exon-6-3′UTR long luciferase activity; comparator: KCl 20 mM alone — RESULTS > Effects of aurora kinases inhibition on BDNF protein production (S96)

In Vivo Studies

Female athymic nude mice bearing subcutaneous p53−/− HCT116 cell xenografts received PHA-680632 at 40 mg kg−1 i.p. b.i.d. for 4 days. PHA-680632 alone produced a marked tumour growth delay compared with the vehicle control. [2]

Tumour growth delay in xenograft models

Animal study · Female athymic nude mice; subcutaneous p53−/− HCT116 cell xenograft models; six mice per group [2]

Female athymic nude mice bearing subcutaneous p53−/− HCT116 cell xenografts received PHA-680632 at 40 mg kg−1 i.p. b.i.d. for 4 days. PHA-680632 alone produced a marked tumour growth delay compared with the vehicle control.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
tumour growth delay (TGD)Reported result A marked tumour growth delay (TGD) was found in animals treated with PHA680632 alone (40 mg kg−1 i.p. b.i.d. for 4 days) compared with the vehicle control.[2]

Conditions shared by the study groups

Route
i.p.
Treatment course
b.i.d. for 4 days
Vehicle
20% Tween-80 in 5% glucose solution
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
PHA-680632 40 mg kg−1vehicle controlA marked tumour growth delay (TGD) was found in animals treated with PHA680632 alone (40 mg kg−1 i.p. b.i.d. for 4 days) compared with the vehicle control.[2]
PHA-680632 40 mg kg−1
Model: Female athymic nude mice; subcutaneous p53−/− HCT116 cell xenograft models; six mice per group
Methods and source locations

Compound reported in the paper: PHA-680632

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

MATERIALS AND METHODS > In vivo xenograft in nude mice (S43, S45, S47, S48); RESULTS > In vivo experiments in subcutaneous xenograft models using the PHA680632 and IR combination (S119, S120)

tumour growth delay (TGD): tumour growth delay (TGD); comparator: vehicle control — RESULTS > In vivo experiments in subcutaneous xenograft models using the PHA680632 and IR combination (S120)

PHA-680632 40 mg kg−1 · RESULTS > In vivo experiments in subcutaneous xenograft models using the PHA680632 and IR combination (S120)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 398493-79-3
Applications Aurora inhibitor
Formula C28H35N7O2
Molecular Weight 501.6
SMILES
CCC1=C(C(=CC=C1)CC)NC(=O)N2CC3=C(C2)NN=C3NC(=O)C4=CC=C(C=C4)N5CCN(CC5)C

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 91 mg/mL (181.41 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
14 mg/mL
Vehicle
5% DMSO+50% PEG 300+5% 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] Polacchini A, Albani C, Baj G, et al. Combined cisplatin and aurora inhibitor treatment increase neuroblastoma cell death but surviving cells overproduce BDNF. Biol Open (2016). PMID: 27256407 DOI: 10.1242/bio.016725 Source material
  2. [2] Tao Y, Zhang P, Frascogna V, et al. Enhancement of radiation response by inhibition of Aurora-A kinase using siRNA or a selective Aurora kinase inhibitor PHA680632 in p53-deficient cancer cells. Br J Cancer (2007). PMID: 18026198 DOI: 10.1038/sj.bjc.6604083 Source material

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