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Fig. 1 · Structure
Cat. No.
A10612
CAS No.
366017-09-6
Formula
C25H23F3N4O2
Mol. Weight
468.5

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Mubritinib (TAK 165)

Cat. No. A10612 CAS 366017-09-6

HER2/ErbB2 inhibitor

Mubritinib (TAK 165) is a potent EGFR and p34cdc2 inhibitor with IC50 of 6 nM and 0.2 μM, respectively. Mubritinib(TAK 165) also inhibits p33cdk2 and p33cdk5.

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Biological Activity

Target & Activity

Target Activity Value
HER2/ErbB2 IC50 6.0nM
EGFR IC50 >25μM
FGFR IC50 >25μM
PDGFR IC50 >25μM
JAK1 IC50 >25μM
Src IC50 >25μM
BLK IC50 >25μM

7 targets · Scroll to view more

Cellular Effect

Cell Line Activity Value Description Reference
A549 IC50 4.27 μM Antiproliferative activity against HER2 weak positive human A549 cells assessed as reduction in cell viability measured after 24 hrs by MTT assay [PMID: 35452936]
BEAS-2B CC50 6.42 μM Cytotoxicity against human BEAS-2B cells assessed as reduction in cell viability measured after 24 hrs by MTT assay [PMID: 35452936]
HepG2 IC50 3.5 μM Antiproliferative activity against HER2 negative human HepG2 cells assessed as reduction in cell viability measured after 24 hrs by MTT assay [PMID: 35452936]
L02 CC50 8.07 μM Cytotoxicity against human L02 cells assessed as reduction in cell viability measured after 24 hrs by MTT assay [PMID: 35452936]
MCF-10A CC50 11.26 μM Cytotoxicity against human MCF-10A cells assessed as reduction in cell viability measured after 24 hrs by MTT assay [PMID: 35452936]
MCF7 IC50 5.75 μM Antiproliferative activity against HER2 negative human MCF7 cells assessed as reduction in cell viability measured after 24 hrs by MTT assay [PMID: 35452936]
MIA PaCa-2 IC50 51 nM Cytotoxicity against human MIA PaCa-2 cells assessed as inhibition of cell growth incubated for overnight in glucose-containing medium followed by compound addition and measured after 7 days by MTT assay [PMID: 35167303]
SK-BR-3 IC50 0.64 μM Antiproliferative activity against human SK-BR-3 cells overexpressing HER2 assessed as reduction in cell viability measured after 24 hrs by MTT assay [PMID: 35452936]

In Vitro Studies

In ES-2 cells, Mubritinib reduced LC3 puncta formation upon autophagy induction by Rapamycin treatment. In model #53, Mubritinib alone reduced the number of live cells to ~35% of control. [1,2]

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

Mubritinib reduces Rapamycin-induced LC3 puncta formation in ES-2 cells

Cell-based study · ES-2 cells [1]

ES-2 cells were treated with Mubritinib and/or Rapamycin. Mubritinib reduced LC3 puncta formation upon autophagy induction by Rapamycin treatment.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
LC3 puncta were quantified by ImageJ software, using at least five different images from two separate experimentsReported result TAK-165 (1 μM), Rapamycin (200 nM), 16 h: TAK-165 reduced LC3 puncta formation upon autophagy induction by Rapamycin treatment in ES-2 cells.[1]

Literature-Reported Treatment Conditions

Treatment concentration
1 μM
Exposure duration
16 h
Co-treatment
Other interventions in this design: Rapamycin 200 nM. Compound effect isolated by the comparison: TAK-165 (1 μM) and/or Rapamycin (200 nM).
Reported limits
Not stated in the sentences used: route, vehicle.
Methods and source locations

Compound reported in the paper: Mubritinib; Compound label in the paper: TAK 165

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

Results > TAK-165 inhibits autophagy in a HER2-independent manner (S41, S45, S48); Material and methods > Immunofluorescence for LC3 puncta formation assay (S124, S125)

LC3 puncta were quantified by ImageJ software, using at least five different images from two separate experiments: LC3 puncta were quantified by ImageJ software, using at least five different images from two separate experiments; comparator: Rapamycin (200 nM) — Results > TAK-165 inhibits autophagy in a HER2-independent manner (S41, S45, S48)

Mubritinib and live cell abundance

Cell-based study · #53 [2]

In model #53, Mubritinib alone or TMZ alone reduced the number of live cells to ~35% or ~50% of the control, respectively.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
cell viability assayscell viability ~35% of the control[2]

Literature-Reported Treatment Conditions

Treatment concentration
500 nM
Exposure duration
Seven days following treatment
Vehicle
0.1% DMSO
Reported limits
Not stated in the sentences used: route.
Methods and source locations

Compound reported in the paper: Mubritinib

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

Results > Combining mubritinib with TMZ chemotherapy effectively suppresses GB growth (S154, S155); Methods > Treatment of BTSCs (S247)

cell viability assays: cell viability assays; comparator: control — Results > Combining mubritinib with TMZ chemotherapy effectively suppresses GB growth (S154, S155)

In Vivo Studies

Mubritinib was administered intraperitoneally to immunodeficient mice bearing intracranial luciferase-expressing BTSC73. Mubritinib monotherapy delayed tumour formation and produced a ~5-fold decrease in luciferase activity compared with vehicle control. [2]

Mubritinib delays tumour formation in an intracranial mouse model

Animal study · luciferase-expressing BTSC73 into the brains of immunodeficient mice [2]

Immunodeficient mice bearing intracranial luciferase-expressing BTSC73 received Mubritinib intraperitoneally at 6 mg/kg. Mubritinib monotherapy delayed tumour formation, with a ~5-fold decrease in luciferase activity compared with vehicle control.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Luciferase imaging at 21 days following surgeryluciferase activity mubritinib (6 mg/kg), 21 days following surgery: ~5-fold decrease in luciferase activity[2]

Conditions shared by the study groups

Route
intraperitoneally injected
Treatment course
7 days after intracranial injection of BTSCs; three times a week (Monday, Wednesday, and Friday) until sacrifice
Vehicle
5% DMSO and corn oil suspension
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Mubritinib 6 mg/kgvehicle controla delay in tumour formation in the group receiving either mubritinib or IR monotherapy, with a ~5-fold decrease in luciferase activity compared to that in the control group[2]
Mubritinib 6 mg/kg
Model: luciferase-expressing BTSC73 into the brains of immunodeficient mice
Methods and source locations

Compound reported in the paper: Mubritinib

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

Results > Combination of mubritinib treatment with IR therapy suppresses GB tumours and improves survival of GB-bearing mice (S103, S104, S106); Methods > Stereotaxic injections and bioluminescent imaging (S392); Methods > Combination of mubritinib and IR in vivo (S396)

Luciferase imaging at 21 days following surgery: Luciferase imaging at 21 days following surgery; comparator: vehicle control — Results > Combination of mubritinib treatment with IR therapy suppresses GB tumours and improves survival of GB-bearing mice (S104, S106)

Mubritinib 6 mg/kg · Results > Combination of mubritinib treatment with IR therapy suppresses GB tumours and improves survival of GB-bearing mice (S104, S106); Methods > Combination of mubritinib and IR in vivo (S396)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 366017-09-6
Applications HER2/ErbB2 inhibitor
Formula C25H23F3N4O2
Molecular Weight 468.5
Synonyms TAK 165
SMILES
C1=CC(=CC=C1CCCCN2C=CN=N2)OCC3=COC(=N3)/C=C/C4=CC=C(C=C4)C(F)(F)F

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 12 mg/mL (25.61 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
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] Ouchida AT, Li Y, Geng J, et al. Synergistic effect of a novel autophagy inhibitor and Quizartinib enhances cancer cell death. Cell Death Dis (2018). PMID: 29374185 DOI: 10.1038/s41419-017-0170-9 Source material
  2. [2] Burban A, Tessier C, Larroquette M, et al. Exploiting metabolic vulnerability in glioblastoma using a brain-penetrant drug with a safe profile. EMBO Mol Med (2025). PMID: 39901019 DOI: 10.1038/s44321-025-00195-6 Source material

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