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Fig. 1 · Structure
Cat. No.
A11051
CAS No.
1110813-31-4
Formula
C24H25ClFN5O2
Mol. Weight
469.9

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Dacomitinib (PF299804, PF299)

Cat. No. A11051 CAS 1110813-31-4

EGFR inhibitor

Dacomitinib (PF299804, PF299) is a potent, orally available, irreversible inhibitor of tyrosine kinase human epidermal growth factor receptors (HER) 1 (EGFR), HER2, and HER4.

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Publications for Dacomitinib

6 publications citing this product

  1. Yuji Uehara, .et al. , Lung Cancer, 2025, Apr:202:108479 PMID: 40088581
  2. Aya Hasan Alshammari, .et al. , Biochem Pharmacol, 2022, Mar;197:114914 PMID: 35041812
  3. Hamzehlou S, .et al. , Eur J Pharmacol, 2019, Nov 15;863:172705 PMID: 31574259
  4. Momeny M, .et al. , Cell Oncol (Dordr), 2019, Apr 25 PMID: 31025257
  5. Majid Momeny, .et al. , Sci Rep, 2017, 7: 4204 PMID: 28646172
  6. Fujita KI, .et al. , J Pharm Sci, 2017, Sep;106(9):2632-2641 PMID: 28479358
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Biological Activity

Bioactivity / Mechanism

In head-and-neck squamous carcinoma cells, dacomitinib suppressed EGF-stimulated EGFR phosphorylation after 24 h exposure. Reported cellular phosphorylation IC50 values were 100 nM in FaDu, 50 nM in UT-SCC-8 and 100 nM in UT-SCC-42a. Downstream signaling was not uniformly suppressed: STAT3 phosphorylation rebounded at higher concentrations. [1]

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

Target & Activity

Target Activity Value
EGFR (Cell-free assay) 6.0 nM
ErbB2 (Cell-free assay) 45.7 nM
ErbB4 (Cell-free assay) 73.7 nM

Cellular Effect

Cell Line Activity Value Description Reference
LoVo IC50 0.011 μM Inhibition of wild type EGFR phosphorylation in human LoVo cells after 2 hrs by fluorescence assay [PMID: 23930994]
NCI-H1975 IC50 0.042 μM Inhibition of EGFR L858R/T970M double mutant phosphorylation in human NCI-H1975 cells after 2 hrs by fluorescence assay [PMID: 23930994]
NCI-H1975 IC50 0.44 μM Antiproliferative activity against human NCI-H1975 cells expressing EGFR T790M/L858R mutant incubated for 72 hrs by MTS assay [PMID: 28754471]
PC-9 IC50 0.00063 μM Inhibition of EGFR exon 19 deletion activating mutant phosphorylation in human PC9 cells after 2 hrs by fluorescence assay [PMID: 23930994]
Sf9 IC50 0.006 μM Irreversible inhibition of GST-tagged ERBB1 (unknown origin) (Met-668 to Ala-1211 residues) expressed in baculovirus infected Sf9 insect cells assessed as reduction in Glu/Tyr copolymer phosphorylation after 6 mins by ELISA [PMID: 27491023]
Sf9 IC50 0.046 μM Irreversible inhibition of GST-tagged ERBB2 (unknown origin) (Ile-675 to Val-1256 residues) expressed in baculovirus infected Sf9 insect cells assessed as reduction in Glu/Tyr copolymer phosphorylation after 6 mins by ELISA [PMID: 27491023]
Sf9 IC50 0.074 μM Irreversible inhibition of GST-tagged ERBB4 (unknown origin) (Gly-259 to Gly-690 residues) expressed in baculovirus infected Sf9 insect cells assessed as reduction in Glu/Tyr copolymer phosphorylation after 6 mins by ELISA [PMID: 27491023]
Sf9 IC50 3.57 μM Irreversible inhibition of human recombinant GST-tagged JAK3 expressed in baculovirus infected Sf9 insect cells assessed as reduction in polyglutamic acid-tyrosine phosphorylation after 30 mins by ELISA [PMID: 27491023]

In Vitro Studies

Dacomitinib (5 μM, 48 h) reduced the MTT proliferation signal in OVCAR3, SKOV3 and A2780CP ovarian carcinoma cells. These findings describe a cellular growth endpoint under the tested conditions; they do not establish a biochemical potency value or a clinical response. [2]

EGF-stimulated signaling in head-and-neck carcinoma cells

Cell-based study · FaDu, UT-SCC-8 and UT-SCC-42a human squamous carcinoma cells [1]

Dacomitinib reduced EGF-stimulated EGFR phosphorylation and downstream ERK, AKT and mTOR phosphorylation. STAT3 behaved differently, with rebound at higher concentrations. These are cellular signaling endpoints, not purified-enzyme inhibition constants.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
EGFR phosphorylation relative to untreated controlCellular phosphorylation IC50 FaDu: 100 nM; UT-SCC-8: 50 nM; UT-SCC-42a: 100 nM[1]
STAT3 phosphorylationQualitative response Reduced at 10 nM; induced above untreated levels at higher concentrations[1]

Literature-Reported Treatment Conditions

Treatment concentration
0, 10, 50, 100, 250 or 500 nM
Exposure duration
24 h; EGF (20 ng/mL) added during the final 30 min
Method
Serum-free exposure followed by Western blotting; phosphorylated and total proteins assessed with β-actin control.
Vehicle
DMSO; shared in-vitro negative control specified as 0.01% DMSO.
Co-treatment
EGF stimulation; no radiation in this signaling experiment.
Reported limits
No exact solid form or lot analytical data. Figure S3 normalization described without numerical underlying densitometry table.
Methods and source locations

Compound reported in the paper: Dacomitinib; Compound label in the paper: PF-00299804

Compound-level published research; no validation of the current A11051 lot or exact solid form.

Figure 4; Results: Dacomitinib inhibited EGFR signalling; Methods: Western Blot Analysis; File S1 Figure S3

EGFR phosphorylation relative to untreated control: Reported densitometry estimates; File S1 S3 normalizes signals to β-actin and phosphorylated/total protein ratios. Representative blots from three independent experiments. — Results: Dacomitinib inhibited EGFR signalling; Figure 4; File S1 Figure S3 and caption

STAT3 phosphorylation: Western blot; representative results from three independent experiments. No exact fold change inferred from image. — Figure 4 and corresponding Results paragraph

Growth inhibition in chemoresistant ovarian carcinoma cells

Cell-based study · OVCAR3, SKOV3 and A2780CP human ovarian carcinoma cells [2]

At 5 μM for 48 h, dacomitinib reduced the MTT proliferation signal in the three ovarian carcinoma models relative to vehicle. Single-targeted comparator agents had weaker effects under their tested conditions. No exact percentage or dacomitinib IC50 is inferred from the bars.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Cell proliferation signal relative to vehicleMTT, qualitative Reduced in OVCAR3, SKOV3 and A2780CP[2]

Literature-Reported Treatment Conditions

Treatment concentration
Dacomitinib 5 μM
Exposure duration
48 h
Method
MTT assay with vehicle-treated control cells.
Vehicle
DMSO; final DMSO did not exceed 0.1% [v/v].
Co-treatment
Dacomitinib alone. Separate comparator treatments: cetuximab, trastuzumab and H3.105.5 each 10 μg/mL; erlotinib 5 μM.
Reported limits
Exact vehicle fraction for this assay and dacomitinib solid form/lot not specified. No exact numerical MTT values tabulated for Figure 3A.
Methods and source locations

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

Compound-level published research; no validation of the current A11051 lot or exact solid form.

Figure 3A; Results: Dacomitinib inhibits cell viability and induces apoptosis; Methods: Antibodies and chemicals, Chemosensitivity assay, Statistical analysis

Cell proliferation signal relative to vehicle: Figure 3A; mean ± SD from three independent experiments, each performed in triplicate. Figure-wide statistical notation is not assigned a new numerical P value here. — Figure 3A image and caption; Methods: Chemosensitivity assay and Statistical analysis

In Vivo Studies

In FaDu-bearing SCID mice, oral dacomitinib at 5 mg/kg/day on days 1–5 increased the mean time to a 14 mm tumor-plus-leg diameter by 13 days versus vehicle. Adding local irradiation (2 Gy on days 2 and 5) increased this delay to 26 days versus vehicle. The size endpoint and combination effect should be distinguished from survival benefit. [1]

FaDu xenograft growth delay with dacomitinib and radiation

Animal study · FaDu xenografts in 6–8-week-old male BALB/c SCID mice [1]

Dacomitinib alone delayed the tumor-plus-leg diameter endpoint relative to DMSO control. Concurrent local irradiation produced a larger delay. The experiment assesses a size endpoint, not clinical survival or eradication.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Increase in mean time to 14 mm tumor-plus-leg diameter versus vehicleTumor growth delay Dacomitinib alone: 13 days (p<0.001); dacomitinib + IR: 26 days (p<0.001)[1]
Body-weight change across four regimensReported fluctuation <15% over the reported 50-day experiment[1]

Conditions shared by the study groups

Vehicle
100% DMSO
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Vehicle control
DMSO only		DMSO-only group; IR-only group provides combination comparator.Comparator for mean time to size endpoint.[1]
Dacomitinib alone
5 mg/kg/day		DMSO-only group; IR-only group provides combination comparator.Mean time to 14 mm tumor-plus-leg diameter increased by 13 days versus vehicle (p<0.001).[1]
Radiation alone
2 Gy/treatment; vehicle administered separately		DMSO-only group; IR-only group provides combination comparator.Growth delay less than the combination; no exact numerical delay inferred.[1]
Dacomitinib plus radiation
Dacomitinib 5 mg/kg/day; local radiation 2 Gy/treatment		DMSO-only group; IR-only group provides combination comparator.Mean time to 14 mm tumor-plus-leg diameter increased by 26 days versus vehicle (p<0.001).[1]
Vehicle control
Model: FaDu xenografts in male BALB/c SCID mice; n = 9/group across three independent experiments
Route: Oral
Frequency: Once daily
Treatment course: Days 1–5
Reported limits: No lot or salt/hydrate identification.
Dacomitinib alone
Model: FaDu xenografts in male BALB/c SCID mice; n = 9/group across three independent experiments
Route: Oral
Frequency: Once daily
Treatment course: Days 1–5
Reported limits: No lot or salt/hydrate identification.
Radiation alone
Model: FaDu xenografts in male BALB/c SCID mice; n = 9/group across three independent experiments
Route: Local tumor irradiation; oral vehicle
Frequency: Two radiation treatments
Treatment course: Radiation days 2 and 5; vehicle days 1–5
Reported limits: No lot or salt/hydrate identification.
Dacomitinib plus radiation
Model: FaDu xenografts in male BALB/c SCID mice; n = 9/group across three independent experiments
Route: Oral dacomitinib; local tumor irradiation
Frequency: Drug once daily; radiation twice during course
Treatment course: Drug days 1–5; radiation days 2 and 5 immediately after dosing
Reported limits: No lot or salt/hydrate identification.
Methods and source locations

Compound reported in the paper: Dacomitinib; Compound label in the paper: PF-00299804

Compound-level published research; no validation of the current A11051 lot or exact solid form.

Figure 6A–B; Results: Combining Dacomitinib and ionizing radiation enhanced tumor growth delay in vivo; Methods: Animal Experiments; File S1 Figure S5

Increase in mean time to 14 mm tumor-plus-leg diameter versus vehicle: Values stated in Results; Fig 6A reports mean ± SEM growth curves, whereas File S1 Fig S5 endpoint scatter reports ± SD; n = 9/group pooled across three experiments. — Results: Combining Dacomitinib and ionizing radiation enhanced tumor growth delay in vivo; Figure 6A; File S1 Figure S5

Body-weight change across four regimens: Figure 6B mean ± SEM; does not establish comprehensive toxicity or safety. — Figure 6B and corresponding Results paragraph

Vehicle control · Figure 6A–B and caption; Methods: Animal Experiments; File S1 Figure S5

Dacomitinib alone · Figure 6A–B and caption; Methods: Animal Experiments; File S1 Figure S5

Radiation alone · Figure 6A–B and caption; Methods: Animal Experiments; File S1 Figure S5

Dacomitinib plus radiation · Figure 6A–B and caption; Methods: Animal Experiments; File S1 Figure S5

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 1110813-31-4
Applications EGFR inhibitor
Formula C24H25ClFN5O2
Molecular Weight 469.9
Synonyms PF-299804; PF-299
SMILES
COC1=C(C=C2C(=C1)N=CN=C2NC3=CC(=C(C=C3)F)Cl)NC(=O)/C=C/CN4CCCCC4

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 17 mg/mL (36.17 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
9 mg/mL
Vehicle
1% DMSO+30% polyethylene glycol+1% Tween 80, pH 9

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] Justin P. Williams, Inki Kim, Emma Ito, et al. Pre-Clinical Characterization of Dacomitinib (PF-00299804), an Irreversible Pan-ErbB Inhibitor, Combined with Ionizing Radiation for Head and Neck Squamous Cell Carcinoma PLoS ONE (2014). PMID: 24853121 DOI: 10.1371/journal.pone.0098557 Source material
  2. [2] Majid Momeny, Ghazaleh Zarrinrad, Farima Moghaddaskho, et al. Dacomitinib, a pan-inhibitor of ErbB receptors, suppresses growth and invasive capacity of chemoresistant ovarian carcinoma cells Scientific Reports (2017). PMID: 28646172 DOI: 10.1038/s41598-017-04147-0 Source material

Publications

6 publications citing this product

  1. Yuji Uehara, .et al. , Lung Cancer, 2025, Apr:202:108479 PMID: 40088581
  2. Aya Hasan Alshammari, .et al. , Biochem Pharmacol, 2022, Mar;197:114914 PMID: 35041812
  3. Hamzehlou S, .et al. , Eur J Pharmacol, 2019, Nov 15;863:172705 PMID: 31574259
  4. Momeny M, .et al. , Cell Oncol (Dordr), 2019, Apr 25 PMID: 31025257
  5. Majid Momeny, .et al. , Sci Rep, 2017, 7: 4204 PMID: 28646172
  6. Fujita KI, .et al. , J Pharm Sci, 2017, Sep;106(9):2632-2641 PMID: 28479358

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