Erlotinib HCl (OSI-744)

Catalog No.S1023 Synonyms: (CP358774, NSC 718781) HCl

Erlotinib HCl (OSI-744) Chemical Structure

Molecular Weight(MW): 429.90

Erlotinib HCl (OSI-744) 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.

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Cited by 74 Publications

17 Customer Reviews

  • Erlotinib IC50 in HCC827 cell lines measured 48h after treatment with vehicle (control) or with erlotinib. Erlotinib IC50 is shown in parentheses. Data are representative of 3 independent experiments. Effects of treatment for 48h with a vehicle or the indicated doses of MP-470 in parental or ER1 and ER2 cell lines in the absence and presence of erlotinib on the indicated biomarkers.

    Nat Genet 2012 44(8):852-60. Erlotinib HCl (OSI-744) purchased from Selleck.

    J Clin Invest 2012 122, 3197-210. Erlotinib HCl (OSI-744) purchased from Selleck.

  • Effects of combined treatment with erlotinib and NPS-1034 in HCC827/ER cells with AXL activation. Lysates were immunoprecipitated with an anti-AXL antibody and immunoblotted with antibodies for phosphotyrosine (p-Tyr) and AXL. HCC827/ER cells were treated with erlotinib. E, erlotinib; N, NPS-1034. **, P < 0.001 for the combination of erlotinib plus NPS-1034 versus either the control or drug alone.

    Cancer Res 2014 4(1):253-62. Erlotinib HCl (OSI-744) purchased from Selleck.

    Immunoblots of MCF7-HER2 cells treated with DMSO (c), BEZ235 (B, 500 nM) and lapatinib (L, 500 nM) as well as with erlotinib (E, 500 nM) and the indicated combinations for 24 h.

     

     

    Oncogene 2010 30, 2547-2557. Erlotinib HCl (OSI-744) purchased from Selleck.

  • (B–C) LNCaP (B) and LNCaP-AI (C) cells were transiently transfected with sPLA2-IIa(-800)-Luc (0.5 μg). The cells were then treated with Erlotinib (20 μM), Gefitinib (20 μM), Lapatinib (20 μM), CI-1033 (8 μM), LY294002 (20 μM) and Bortezomib (20 μM) without or with EGF (100 ng/ml) for 24 h. Luciferase assay was performed according to a standard protocol with Renilla luciferase as an internal control. Data are presented as the mean (±SD) of duplicate values of a representative experiment that was independently repeated for five times.

    Carcinogenesis 2010 31, 1948–1955. Erlotinib HCl (OSI-744) purchased from Selleck.

    LNCaP-AI cells were starved in 1% stripped medium for 24 h. The cells were then treated with Erlotinib (20 μM), Gefitinib (20 μM), Lapatinib (20 μM), CI-1033 (8 μM), LY294002 (20 μM) and Bortezomib (20 μM) for 24 h. Cell culture medium was collected from each sample and subjected to ELISA for sPLA2-IIa. The condition medium samples were diluted 10 times for ELISA. Average of duplicate samples was converted to nanogram per milliliter against standard curve. The data represent one of five repeated experiments.

     

     

    Carcinogenesis 2010 31, 1948–1955. Erlotinib HCl (OSI-744) purchased from Selleck.

  • Susceptibility of lung cancer cells to cytolytic activity of NK-92 cells after treatment with EGFR inhibitors. Three lung cancer cells were untreated (open circle) or treated with 10 μM erlotinib or gefitinib (black filled square or black filled triangle) for 24 hours. The lung cancer cells were cocultured with NK-92 cells at indicated effector to target ratio (E:T ratio). To determine the specificity of NKG2D-mediated cytolysis of lung cancer cells, NK-92 cells were preincubated with blocking mAb against NKG2D before the assay (gray filled square and triangle) and correspond-ing isotype mAb (open square and triangle).

    J Immunother 2011 34, 372-81. Erlotinib HCl (OSI-744) purchased from Selleck.

     

    The TMZ-induced caveolin-1 modulation is Src-dependent in Hs683 GBM cells Western blot analyses of soluble caveolin-1 expression in Hs683 glioma cells treated with TMZ (100 μM) four times per week (day 1-4) for 7 h/d, the EGFR inhibitor (10 μM) (erlotinib; day 1), the Src inhibitor AZD0530 (10 μM) (day 1), and combination of the inhibitors and TMZ (+TMZ) compared with control untreated cells (Ct). Soluble caveolin-1 expression was measured on day 5.

    Transl Oncol 2011 4, 92-100. Erlotinib HCl (OSI-744) purchased from Selleck.

  • miR-17-5p is down-regulated by erlotinib treatment in A549-ER cells. (A) MTT was used to assess cell viability of A549 and A549-ER cells after 72-h erlotinib treatment with different concentrations. (B) Real-time PCR quantification of indicated miRNAs. (C) Real-time PCR quantification of miR-17-5p in A549 cells treated with erlotinib at indicated concentrations for 48 h. For all, *p < 0.05, **p < 0.01, ***p < 0.001versus control group.

    J Drug Target, 2016, 25(2):125-131. Erlotinib HCl (OSI-744) purchased from Selleck.

    Pressure-induced myogenic tone in coronary arterioles with and without EGFR tyrosine kinase inhibitors (AG1478 and Erlotinib, 1 μM) n=6, *Pb0.05 CTR vs. EGFR inhibitor

     

     

    Microvasc Res 2010 81, 135-142. Erlotinib HCl (OSI-744) purchased from Selleck.

  • PAS staining and Masson's trichrome staining of kidneys in 22-week-old vehicleor erlotinib-treated AS mice.

    Clin Exp Nephrol, 2017.. Erlotinib HCl (OSI-744) purchased from Selleck.

    Tuberc Respir Dis 2013 75(1), 9-17. Erlotinib HCl (OSI-744) purchased from Selleck.

  • Erlotinib and picropodophyllin (PPP) act together to reduce cell proliferation. MET1 cells were cultured for 48 hours in increasing concentrations of erlotinib (A) or PPP (B) as indicated. Cell growth was then assessed using methyl thiazolyl-tetrazolium (MTT) assays. A dose-dependent decrease in the number of viable cells is seen with rising inhibitor concentrations (n = 3 at all time points). MET1 cells (C), MET4 cells (D), SCC12 cells (E), and SCC13 cells (F) were cultured for 48 hours in varying concentrations of erlotinib and PPP as indicated. Cell growth was then assayed with MTT assays. Both erlotinib and PPP demonstrated dose-dependent inhibition of cell growth, and at intermediate concentrations there seemed to be synergistic prevention of cell growth by both inhibitors. Higher concentrations of all inhibitors were also tested but are not shown as they exceeded the maximal responses of the cells to the inhibitors.

    Head Neck 2013 35, 86-93. Erlotinib HCl (OSI-744) purchased from Selleck.

    Inhibition of anchorage-independent growth of lung tumor cell lines by selected inhibitors. Each selected cell line was treated with the indicated inhibitor at 0.1 μM and 1 μM concentrations for two weeks and cell colony size formation was scored under the Nikon inverted-phase microscope.

    Int J Proteomics 2011 2011, Article ID 215496. Erlotinib HCl (OSI-744) purchased from Selleck.

  • DUSP6 is regulated by EGFR/ERK inhibition in NSCLC cell lines. Protein expression levels were assayed by immunoblot for phosphor-EGFR at indicated tyrosine sites, total-EGFR, phosphor-ERK, total-ERK, ETS1, DUSP6 and GAPDH demonstrating suppression of DUSP6 following inhibition of activated ERK (P-ERK) and ETS1 levels in the presence of appropriate drug for each of the following cell lines: (a) HCC827 cells treated with erlotinib; (b) H1975 cells treated with erlotinib or CL-387,785 (an irreversible EGFR inhibitor); H441 cells treated with (c) erlotinib or U0126 (a MEK1/2 inhibitor) and (d) erlotinib or AG1478 (specific EGFR inhibitor) (d). Cells were starved overnight with serum-free media, then treated with drug as indicated by the following abbreviations: (E) 100ng/ml EGF; (D) 0.01% DMSO control; (Er) 1 μM erlotinib, (CL) 1 μM CL-387,785, (U) 20 μM U0126 or AG1478. Whole cell lysates were obtained using 10% TCA lysis buffer and immunoblotting was performed at indicated time points.

     

     

    2010 Dr. Balazs Halmos of Columbia University. Erlotinib HCl (OSI-744) purchased from Selleck.

    DUSP6 gene expression is inhibited by erlotinib using quantitative real-time PCR analysis. RNA was extracted from treated (a) HCC827 and (b) PC9 cells and relative expression level standardized against GAPDH at several time points.

     

     

    2010 Dr. Balazs Halmos of Columbia University. Erlotinib HCl (OSI-744) purchased from Selleck.

  • Breast cancer cells were pretreated with 100ng/ml EGF for 15 min and then treated with the indicated concentrations of  Erlotinib for 24 hours.

     

     

    2010 Dr. Zhang of Tianjin Medical University. Erlotinib HCl (OSI-744) purchased from Selleck.

Purity & Quality Control

Choose Selective EGFR Inhibitors

Biological Activity

Description Erlotinib HCl (OSI-744) 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]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human A431 cells M3\VOWZ2dmO2aX;uJIF{e2G7 MYjJcohq[mm2aX;uJI9nKEWJRmKgbY4hcHWvYX6gRVQ{OSClZXzsd{BjgSCKVGLGJIF{e2G7LDDJR|UxRTBwNEKg{txONg>? MmDrNVk5OTV2MUK=
human SKBR3 cells MXfGeY5kfGmxbjDhd5NigQ>? NFnvSVFKdmirYnn0bY9vKG:oIFjFVlIhcW5iaIXtZY4hW0uEUkOgZ4VtdHNiYomgTHRTTiCjc4PhfUwhUUN3ME2xMlg6KM7:TT6= MXOxPVgyPTRzMh?=

... Click to View More Cell Line Experimental Data

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

Kinase Assay:[1]
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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 Research:[2]
+ Expand
  • 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.
    (Only for Reference)
Animal Research:[6]
+ Expand
  • Animal Models: Male 5-week-old BALB-nu/nu with HPAC cells
  • Formulation: 6% Captisol
  • Dosages: 50 mg/kg
  • Administration: Oral administration
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 4 mg/mL warmed (9.3 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents individually and in order:
15% Captisol
16 mg/mL warmed (suspension)

* 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.

Chemical Information

Molecular Weight 429.90
Formula

C22H23N3O4.HCl

CAS No. 183319-69-9
Storage powder
Synonyms (CP358774, NSC 718781) HCl

Bio Calculators

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02689336 Recruiting Glioma|Rhabdomyosarcoma|Osteosarcoma|Medulloblastoma|Neuroectodermal Tumor|Ependymoma|Ewings Sarcoma|Wilms Tumor Washington University School of Medicine August 6, 2016 Phase 2
NCT01130519 Recruiting HLRCC|Metastatic Papillary RCC National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) May 4, 2010 Phase 2
NCT01306045 Recruiting Carcinoma, Non-Small-Cell Lung|Carcinoma, Small Cell Lung|Carcinoma, Thymic National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) January 21, 2011 Phase 2
NCT02961374 Not yet recruiting Attenuated Familial Adenomatous Polyposis|Familial Adenomatous Polyposis National Cancer Institute (NCI) January 2017 Phase 2
NCT02942095 Not yet recruiting Solid Tumors M.D. Anderson Cancer Center|Millennium: The Takeda Oncology Company December 2016 Phase 1
NCT02925234 Recruiting Cancer|Tumors|Neoplasm|Neoplasia The Netherlands Cancer Institute|Amgen|AstraZeneca|Bayer|Bristol-Myers Squibb|Novartis|Roche Pharma AG August 2016 Phase 2

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

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Frequently Asked Questions

  • Question 1:

    Whether S1023 is suitable for mouse assays?

  • Answer:

    Dissolving S1023 in 15% Captisol is for oral gavage and it's a suspension.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID