Erlotinib HCl

Catalog No.S1023 Batch:S102303

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Technical Data

Formula

C22H23N3O4.HCl
Molecular Weight 429.90 CAS No. 183319-69-9
Solubility (25°C)* In vitro DMSO 6 mg/mL (13.95 mM)
Water Insoluble
Ethanol Insoluble
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Biological Activity

Description Erlotinib HCl is an EGFR inhibitor with IC50 of 2 nM in cell-free assays, >1000-fold more sensitive for EGFR than human c-Src or v-Abl.
Targets
HER1/EGFR [1]
(Cell-free assay)
2 nM
In vitro Erlotinib HCl potently inhibits EGFR activation in intact cells including HNS human head and neck tumor cells (IC50 20nM), DiFi humancolon cancer cells andMDA MB-468 human breast cancer cells. Erlotinib HCl (1 μM) induces apoptosis in DiFi humancolon cancer cells. [1] Erlotinib inhibits growth of a panel of NSCLC cell lines including A549, H322, H3255, H358 H661, H1650, H1975, H1299, H596 with IC50 ranging from 29 nM to >20 μM. [2] Erlotinib HCl(2 μM) significantly inhibits growth of AsPC-1 and BxPC-3 pancreatic cells. [3] The effects of Erlotinib HCl in combination with gemcitabine are considered additive in KRAS-mutated pancreatic cancer cells. Ten micromolar of Erlotinib HCl inhibits EGFR phospho-rylation at the Y845 (Src-dependent phosphorylation) and Y1068 (auto-phosphorylation) sites. [4] Combination with Erlotinib HCl could down-modulate rapamycin-stimulated Akt activity and produces a synergistic effect on cell growth inhibition. [5]
In vivo At doses of 100 mg/kg, Erlotinib HCl completely prevents EGF-induced autophosphorylation of EGFR in human HN5 tumors growing as xenografts in athymic mice and of the hepatic EGFR of the treated mice. [1] Erlotinib HCl (100 mg/Kg) inhibits H460a and A549 tumor models with 71 and 93% inhibition rate. [5]

Protocol (from reference)

Kinase Assay:[1]
  • Kinase assays

    96-well plates are coated by incubation overnight at 37 °C with 100 μL per well of 0.25 mg/mL PGT in PBS. Excess PGT is removed by aspiration, and the plate is washed 3 times with washing buffer (0.1% Tween 20 in PBS). The kinase reaction is performed in 50 μL of 50 mM HEPES (pH 7.3), containing 125 mM sodium chloride, 24 mM magnesium chloride, 0.1 mM sodium orthovanadate, 20 μM ATP, 1.6 μg/mL EGF, and 15 ng of EGFR, affinity purified from A431 cell membranes. Erlotinib HCl in DMSO is added to give a final DMSO concentration of 2.5%. Phosphorylation is initiated by addition of ATP and proceeded for 8 minutes at room temperature, with constant shaking. The kinase reaction is terminated by aspiration of the reaction mixture and is washed 4 times with washing buffer. Phosphorylated PGT is measured by 25 minutes of incubation with 50 μL per well HRP-conjugated PY54 antiphosphotyrosine antibody, diluted to 0.2 μg/mL in blocking buffer (3% BSA and 0.05% Tween 20 in PBS). Antibody is removed by aspiration, and the plate is washed 4 times with washing buffer. The colonmetric signal is developed by addition of TMB Microwell Peroxidase Substrate, 50μL per well, and stopped by the addition of 0.09 M sulfuric acid, 50 μL per well. Phosphotyrosine is estimated by measurement of absorbance at 450 nm. The signal for controls is typically 0.6-1.2 absorbance units, with essentially no back ground in wells without AlP, EGFR, or PGT and is proportional to the time of incubation for 10 minutes.
Cell Assay:[2]
  • Cell lines

    A549, H322, H3255, H358 H661, H1650, H1975, H1299, H596 cells

  • Concentrations

    30 nM-20 μM

  • Incubation Time

    72 hours

  • Method

    Exponentially growing cells are seeded in 96-well plastic plates and exposed to serial dilutions of erlotinib, pemetrexed, or the combination at a constant concentration ratio of 4:1 in triplicates for 72 h. Cell viability is assayed by cell count and the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Growth inhibition is expressed as the percentage of surviving cells in drug-treated versus PBS-treated control cells (which is considered as 100% viability). The IC50 value is the concentration resulting in 50% cell growth inhibition by a 72-h exposure to drug(s) compared with untreated control cells and is calculated by the CalcuSyn software.
Animal Study:[6]
  • Animal Models

    Male 5-week-old BALB-nu/nu with HPAC cells

  • Dosages

    50 mg/kg

  • Administration

    Oral administration

Customer Product Validation

Data from [Cancer Res, 2014, 4(1):253-62]

Data from [Tuberc Respir Dis, 2013, 75(1), 9-17]

Data from [Head Neck, 2013, 35, 86-93]

Data from [Nat Genet, 2012, 44(8):852-60]

Selleck's Erlotinib HCl has been cited by 599 publications

Cellular mechanisms of heterogeneity in NF2-mutant schwannoma [ Nat Commun, 2023, 14(1):1559] PubMed: 36944680
SPINK1-induced tumor plasticity provides a therapeutic window for chemotherapy in hepatocellular carcinoma [ Nat Commun, 2023, 14(1):7863] PubMed: 38030644
mTOR inhibition reprograms cellular proteostasis by regulating eIF3D-mediated selective mRNA translation and promotes cell phenotype switching [ Cell Rep, 2023, 42(8):112868] PubMed: 37494188
Autocrine activation of MAPK signaling mediates intrinsic tolerance to androgen deprivation in LY6D prostate cancer cells [ Cell Rep, 2023, 42(4):112377] PubMed: 37060563
Increased EGFRvIII Epitope Accessibility after Tyrosine Kinase Inhibitor Treatment of Glioblastoma Cells Creates More Opportunities for Immunotherapy [ Int J Mol Sci, 2023, 24(5)4350] PubMed: 36901782
MEK Is a Potential Indirect Target in Subtypes of Head and Neck Cancers [ Int J Mol Sci, 2023, 24(3)2782] PubMed: 36769112
Multiscale Analysis and Validation of Effective Drug Combinations Targeting Driver KRAS Mutations in Non-Small Cell Lung Cancer [ Int J Mol Sci, 2023, 24(2)997] PubMed: 36674513
Inhibition of VEGFR2 and EGFR signaling cooperatively suppresses the proliferation of oral squamous cell carcinoma [ Cancer Med, 2023, 12(15):16416-16430] PubMed: 37341071
Inhibition of VEGFR2 and EGFR signaling cooperatively suppresses the proliferation of oral squamous cell carcinoma [ Cancer Med, 2023, 12(15):16416-16430] PubMed: 37341071
Genome-wide epigenetic and mRNA-expression profiling followed by CRISPR/Cas9-mediated gene-disruptions corroborate the MIR141/MIR200C-ZEB1/ZEB2-FGFR1 axis in acquired EMT-associated EGFR TKI-resistance in NSCLC cells [ Transl Lung Cancer Res, 2023, 12(1):42-65] PubMed: 36762066

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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

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