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Erlotinib (OSI744, Tarceva)

Alias: Erlotinib free base; NSC718781; NSC718781; CP358774; OSI-774; OSI 774; NSC 718781; CP-358,774; CP-358774; OSI774
Cat No.:V0544 Purity: ≥98%
Erlotinib (formerly OSI744, trade name:Tarceva) isa quinazoline-based EGFR (epidermal growth factor receptor) inhibitor with potential antineoplastic activity.
Erlotinib (OSI744, Tarceva)
Erlotinib (OSI744, Tarceva) Chemical Structure CAS No.: 183321-74-6
Product category: EGFR
This product is for research use only, not for human use. We do not sell to patients.
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Other Forms of Erlotinib (OSI744, Tarceva):

  • Erlotinib HCl (OSI-744, Tarceva)
  • Erlotinib mesylate
  • Erlotinib D6 (CP-358774 D6; NSC-718781 D6; OSI-774 D6)
  • Erlotinib-13C6 (CP-358774-13C6; NSC 718781-13C6; OSI-774-13C6)
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Top Publications Citing lnvivochem Products
InvivoChem's Erlotinib (OSI744, Tarceva) has been cited by 1 publication
Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Erlotinib (formerly OSI744, trade name: Tarceva) is a quinazoline-based EGFR (epidermal growth factor receptor) inhibitor with potential antineoplastic activity. In cell-free experiments, it inhibits EGFR with an IC50 of 2 nM, and compared to human c-Src or v-Abl, it is >1000 times more sensitive to EGFR. Pancreatic cancer, non-small cell lung cancer (NSCLC), and various other cancers can be treated with erlotinib, a medication that has FDA approval. It inhibits EGFR phosphorylation and prevents the signal transduction pathways and carcinogenic consequences linked to EGFR activation by competing with adenosine triphosphate and reversibly binding to the intracellular catalytic domain of EGFR tyrosine kinase.

Biological Activity I Assay Protocols (From Reference)
Targets
EGFR (IC50 = 2 nM)
ln Vitro
Erlotinib (CP-358774) is also a potent inhibitor, with an IC50 of 1 nM, of the EGFR's recombinant intracellular (kinase) domain. Erlotinib severely inhibits the proliferation of DiFi cells, with an IC50 of 100 nM for an 8-day proliferation assay[1]. When B-DIM and Erlotinib (2 μM) are combined, BxPC-3 cell colony formation is significantly inhibited as opposed to when either agent is used alone. Only in BxPC-3 cells does the combination of B-DIM and Erlotinib (2 μM) significantly induce apoptosis when compared to the apoptotic effect of either agent alone[2].
The epidermal growth factor receptor (EGFR) is overexpressed in a significant percentage of carcinomas and contributes to the malignant phenotype. CP-358,774 is a directly acting inhibitor of human EGFR tyrosine kinase with an IC50 of 2 nM and reduces EGFR autophosphorylation in intact tumor cells with an IC50 of 20 nM. This inhibition is selective for EGFR tyrosine kinase relative to other tyrosine kinases we have examined, both in assays of isolated kinases and whole cells. At doses of 100 mg/kg, CP-358,774 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. CP-358,774 inhibits the proliferation of DiFi human colon tumor cells at submicromolar concentrations in cell culture and blocks cell cycle progression at the G1 phase. This inhibitor produces a marked accumulation of retinoblastoma protein in its underphosphorylated form and accumulation of p27KIP1 in DiFi cells, which may contribute to the cell cycle block. Inhibition of the EGFR also triggers apoptosis in these cells as determined by formation of DNA fragments and other criteria. These results indicate that CP-358,774 has potential for the treatment of tumors that are dependent on the EGFR pathway for proliferation or survival. [1]
Effects of B-DIM and Erlotinib on the Viability of Pancreatic Cancer Cells [2]
It is important to note that, during our pilot studies, as indicated in Materials and Methods, different concentrations of B-DIM and erlotinib were used and are presented in Table 1. Moreover, after analyzing the basal level of expression of EGFR, NF-κB, and COX-2, we chose two cell lines having constitutively activated levels of NF-κB, EGFR, and COX-2 expression (BxPC-3) compared with lower level of NF-κB, EGFR, and COX-2 expression (MIAPaCa). Our results prompted us to select the subsequent concentration of B-DIM and erlotinib as presented below. Cell viability of BxPC-3 and MIAPaCa pancreatic cancer cells treated with B-DIM (20 µmol/L), erlotinib (2 µmol/L), and the combination was determined by the MTT assay, and the data are presented in Fig. 1A and B. Significant inhibition of cell viability was seen in BxPC-3 cells treated with either agent, and this was further enhanced by the combination treatment (P = 0.0001). In addition, we have also tested the effects of treatment on cell viability by clonogenic assay as shown below. Similar treatments of MIAPaCa cells resulted in a significant inhibition of viable cells with B-DIM alone but not when exposed to similar concentrations of B-DIM and erlotinib for the same time, and the effect was not enhanced by the combination treatment (P = 0.0890). The insensitivity of MIAPaCa cells to erlotinib is consistent with a recently published report
Inhibition of Cell Growth/Survival by Clonogenic Assay [2]
To determine the effect of B-DIM and Erlotinib on cell growth, cells were treated with each of the single agents or their combination and assessed for cell viability by clonogenic assay. The combination of B-DIM and erlotinib resulted in a significant inhibition of colony formation in BxPC-3 cells when compared with either agent alone (Fig. 2A and B). Similar treatment of MIAPaCa cells (Fig. 2C) showed inhibition of colony formation with B-DIM alone and also the combination, but the effect was not enhanced with the combination treatment as was seen in BxPC-3 cells (Fig. 2A and B). These results were similar to those obtained from the soft-agar assay. Overall, the results from clonogenic assay was consistent with the MTT data as shown in Fig. 1A and B, suggesting that B-DIM had a differential effect between BxPC-3 and MIAPaCa pancreatic cancer cells. The mechanisms of such differences were further investigated, and the results are presented in the following sections, but first we have determined the effects of B-DIM, erlotinib, and the combination on apoptotic cell death.
Induction of Apoptosis by Erlotinib, B-DIM, and the Combination [2]
The underlying mechanism on the inhibition of cell viability was further studied by determining the apoptotic effects of different treatments using the Cell Death Detection ELISA. The combination of B-DIM and erlotinib resulted in a significant induction of apoptosis only in BxPC-3 cells when compared with the apoptotic effect of either agent alone (Fig. 1C). Similar treatment of MIAPaCa cells showed no induction of apoptosis with the combination (Fig. 1D). These results are consistent with cell viability assay by MTT. Subsequently, we sought to find further evidence of apoptosis as presented below.
B-DIM Enhances Apoptosis Signaling by Erlotinib [2]
PARP cleavage was determined in BxPC-3 and MIAPaCa cells that were treated with B-DIM (20 µmol/L), erlotinib (2 µmol/L), and the combination (Fig. 3). We found significant amount of PARP (116 kDa) protein cleavage product (85 kDa fragment) after 72-h treatment only in BxPC-3 cells (Fig. 3). In contrast, MIAPaCa cells treated similarly showed only a small cleavage of PARP with B-DIM alone and also in combination but not with erlotinib alone. The induction of apoptosis could be partly due to inactivation of important survival genes; hence, we investigated whether B-DIM, erlotinib, and their combination could affect key survival proteins.
Effect of B-DIM on Molecules Related to Apoptosis [2]
BxPC-3 and MIAPaCa cells were used to evaluate the effects of B-DIM and/or Erlotinib on the expression of survivin, Bcl-2, Bcl-xL, and c-IAP1/2. Expression of Bcl-2, Bcl-xL, survivin, and c-IAP1/2 proteins was significantly reduced in cells treated with the combination when compared with either agent alone (Fig. 3). There was no influence on antiapoptotic proteins in MIAPaCa cells treated with either agent alone or the combination. These results suggest that B-DIM, erlotinib, and the combination down-regulate key survival proteins and in turn induced apoptotic cell death in BxPC-3 cells but not in MIAPaCa cells. To further determine the molecular mechanism by which B-DIM sensitized BxPC-3 cells to erlotinib-induced inhibition of cell viability and induction of apoptosis, we investigated the role of EGFR and its downstream signaling pathways.
Effect of B-DIM on the Expression of EGFR Protein [2]
The expression of EGFR was determined by immunoblotting. No baseline expression of EGFR was found in the MIAPaCa cells. EGFR-expressing BxPC-3 cells showed a significant reduction in the expression of EGFR and phosphorylated EGFR levels when exposed to erlotinib plus B-DIM compared with either agent alone (Fig. 3). It is known that the activation of EGFR could in turn regulate an important transcription factor, NF-κB, which is a known regulator of several survival genes such as survivin, c-IAP1/2, Bcl-2, and Bcl-xL. Because we found a greater degree of down-regulation of survivin, c-IAP1/2, Bcl-2, and Bcl-xL in BxPC-3 cells treated with B-DIM and erlotinib compared with either agent alone, and because these genes are transcriptionally regulated by NF-κB, we investigated the effect of each treatment on the DNA-binding activity of NF-κB.
B-DIM Inhibits NF-κBDNA-Binding Activity [2]
The activation of NF-κB, a nuclear transcriptional factor, was assessed in B-DIM-treated and Erlotinib-treated cells. There was a significant inhibition of NF-κB activation in BxPC-3 cells exposed to both erlotinib and B-DIM compared with erlotinib alone (Fig. 4A). No such inhibition was shown in the MIAPaCa cells (Fig. 4B). These results suggest that the combination of B-DIM and erlotinib causes greater inhibition of cell growth, induction of apoptosis, inhibition of survival factors, inhibition of EGFR, and inactivation of NF-κB.
Because NF-κB plays important roles in the regulation of prosurvival and antiapoptotic processes, we tested whether overexpression of NF-κB by p65 cDNA transfection could abrogate B-DIM-induced and erlotinib-induced apoptotic processes. Moreover, it is known that NF-κB transcriptionally regulates COX-2, which produces PGE2 and in turn induces cell viability. Thus, we tested whether celecoxib, erlotinib, or B-DIM alone could influence the activity of B-DIM and erlotinib in p65 cDNA transfected cells.
Erlotinib, B-DIM, and Celecoxib Abrogated Activation of NF-κBActivity Stimulated by p65 cDNA Transfection [2]
Cytoplasmic and nuclear proteins from BxPC-3 and MIAPaCa cells transfected with p65 cDNA and then treated with erlotinib (2 µmol/L), B-DIM (20 µmol/L), or celecoxib (5 µmol/L) or left untreated for 48 h were subjected to analysis for NF-κB activity as measured by Western blot analysis and EMSA. The results showed that erlotinib, B-DIM, and celecoxib inhibited the p65 protein and NF-κB DNA-binding activity more in BxPC-3 cells compared with untreated cells (Fig. 5A and B) and very little effect was seen in MIAPaCa cells. Importantly, NF-κB p65 cDNA transfection enhanced the NF-κB p65 protein and DNA-binding activity only in BxPC-3 cells to a significant level as shown in Fig. 5A and B. On the other hand, no such changes were observed in the MIAPaCa cells. Because the activation of NF-κB induces COX-2 expression leading to the production of PGE2 that is released into the culture medium, we measured the levels of PGE2 in untransfected and transfected cells treated with erlotinib, B-DIM, and the COX-2 inhibitor celecoxib.
Inhibition of PGE2 Synthesis in p65 cDNA-Transfected Cells [2]
We measured the levels of PGE2 in the conditioned medium collected from both BxPC-3 and MIAPaCa cells as an indicator of COX-2 activity. We found a high level of PGE2 secretion by BxPC-3 cells, whereas MIAPaCa cells showed very low levels of PGE2, which is consistent with its low constitutive expression of COX-2. BxPC-3 and MIAPaCa cells were transfected with p65 cDNA followed by treatment with Erlotinib (10 nmol/L), B-DIM (1 µmol/L), or celecoxib (1 nmol/L) to analyze the levels of PGE2 released into the culture medium (Fig. 5C). No change in PGE2 level was noted when cells were treated with erlotinib alone (P = 0.084). However, a significant reduction in PGE2 level was observed in BxPC-3 cells treated with B-DIM (P = 0.006) and celecoxib (P = 0.005). There was a substantial increase in the PGE2 level in p65 cDNA-transfected BxPC-3 cells compared with untransfected cells (P = 0.009), suggesting that NF-κB could induce COX-2 expression. However, there was no change in PGE2 level in MIAPaCa cells with any of the agents. Collectively, these results suggest that the production of PGE2 is mediated through the NF-κB and COX-2 pathway and that celecoxib could down-regulate both NF-κB and COX-2. These results were subsequently correlated with the degree of apoptosis (Fig. 5D) as presented below.
Apoptosis through the Inactivation of NF-κB in p65 cDNA-Transfected Cells [1]
p65 cDNA was transfected into BxPC-3 and MIAPaCa cells and then treated with Erlotinib (2 µmol/L), B-DIM (20 µmol/L), or celecoxib (5 µmol/L) for 48 h (Fig. 5D). The degree of apoptosis in p65 cDNA-transfected BxPC-3 cells treated with erlotinib (P = 0.034) was much less compared with untransfected cells treated with erlotinib (P = 0.007). Similar results were observed with both B-DIM and celecoxib treatment in BxPC-3 cells. However, in MIAPaCa cells, no such degree of apoptosis was observed. These results suggest that activation of NF-κB by p65 cDNA transfection could abrogate the apoptosis inducing effect of erlotinib, B-DIM, and celecoxib.
ln Vivo
In comparison to the untreated control, the combination of B-DIM and Erlotinib (50 mg/kg, i.p.) treatment significantly (P <0.01) reduces tumor weight under experimental conditions[2]. In comparison to the CP+vehicle (V) rats, erlotinib (20 mg/kg, p.o.) significantly attenuates the body weight (BW) loss induced by Cisplatin (CP) (P<0.05). Treatment with erlotinib considerably enhances renal function in CP-N (normal control group, NC) rats. Compared to the CP+V rats, the CP+Erlotinib (E) rats exhibit a significant increase in urine volume (UV) (P<0.05) and Cr clearance (Ccr) (P<0.05), as well as a significant decrease in serum creatinine (s-Cr) (P<0.05), blood urea nitrogen (BUN) (P<0.05), and urinary N-acetyl-β-D-glucosaminidase (NAG) index (P<0.05).
B-DIM Augments In vivo Therapeutic Effect of Erlotinib on Primary Tumor [2]
Potential therapeutic utility of B-DIM and erlotinib combination in SCID mice bearing orthotopically implanted BxPC-3 pancreatic tumor cells was investigated. A dose of 3.5 mg/d B-DIM per mouse was selected for p.o. administration, whereas erlotinib dose (50 mg/kg body weight i.p.) was based on previously published reports as shown in Fig. 6A. A total of 28 mice were divided into four groups. To ascertain the efficacy of a single-agent treatment compared with combinations, we determined the mean pancreas weight in all treated groups. Under our experimental conditions, administration of B-DIM by gavage treatment and erlotinib alone caused 20% and 35% reduction in tumor weight, respectively, compared with control tumors (Fig. 6C). However, under the experimental conditions, the combination of B-DIM and erlotinib treatment showed significant decrease (P < 0.01) in tumor weight compared with untreated control, B-DIM alone, or erlotinib alone treatment group. These results showed, for the first time, the efficacy of combination of B-DIM and erlotinib in the inhibition of pancreatic tumor growth in an orthotopic model.
B-DIM Inhibits NF-κBDNA-Binding Activity In vivo [2]
The activation of NF-κB was assessed in B-DIM-treated and Erlotinib-treated tumor tissues. The results show that NF-κB was down-regulated by B-DIM and erlotinib (Fig. 6B). Fig. 6B (bottom) represents results from all seven mice. These in vivo results were similar to our in vitro findings, suggesting that the inactivation of NF-κB is, at least, one of the molecular mechanisms by which B-DIM potentiates erlotinib-induced antitumor activity in our experimental animal model.
The effects of blocking the epidermal growth factor receptor (EGFR) in acute kidney injury (AKI) are controversial. Here we investigated the renoprotective effect of Erlotinib, a selective tyrosine kinase inhibitor that can block EGFR activity, on cisplatin (CP)-induced AKI. Groups of animals were given either Erlotinib or vehicle from one day before up to Day 3 following induction of CP-nephrotoxicity (CP-N). In addition, we analyzed the effects of erlotinib on signaling pathways involved in CP-N by using human renal proximal tubular cells (HK-2). Compared to controls, rats treated with erlotinib exhibited significant improvement of renal function and attenuation of tubulointerstitial injury, and reduced the number of apoptotic and proliferating cells. Erlotinib-treated rats had a significant reduction of renal cortical mRNA for profibrogenic genes. The Bax/Bcl-2 mRNA and protein ratios were significantly reduced by erlotinib treatment. In vitro, we observed that erlotinib significantly reduced the phosphorylation of MEK1 and Akt, processes that were induced by CP in HK-2. Taken together, these data indicate that erlotinib has renoprotective properties that are likely mediated through decreases in the apoptosis and proliferation of tubular cells, effects that reflect inhibition of downstream signaling pathways of EGFR. These results suggest that erlotinib may be useful for preventing AKI in patients receiving CP chemotherapy[3].
Enzyme Assay
The kinase reaction takes place in 50 μL of 50 mM HEPES (pH 7.3), which also contains 15 ng of affinity-purified EGFR from A431 cell membranes, 1.6 μg/mL EGF, 0.1 mM Na3VO4, 125 mM NaCl, and 20 μM ATP. To achieve a final DMSO concentration of 2.5%, the compound is added to DMSO. The addition of ATP starts the phosphorylation process, which lasts for 8 mm at room temperature while being constantly shaken. The reaction mixture is aspirated to stop the kinase reaction, and wash buffer is used four times over. Phosphorylated PGT is quantified after 25 microseconds of incubation with 50 microliters of HRP-conjugated PY54 antiphosphotyrosine antibody per well, diluted to 0.2 micrograms/mL in blocking buffer (PBS containing 3% BSA and 0.05% Tween 20). After aspirating out the antibody, the plate is cleaned four times using wash buffer. TMB Microwell Peroxidase Substrate, 50 μL per well, is added to develop the colonmetric signal.0.09 M sulfuric acid, 50 μL per well, is added to stop the signal. The absorbance at 450 nm is used to estimate phosphotyrosine. The signal for controls is proportional to the incubation time for 10 mm and usually ranges from 0.6 to 1.2 absorbance units[1]. In wells devoid of AlP, EGFR, or POT, there is essentially no background signal.
Cell Assay
In order to assess the survival of cells treated with B-DIM, Erlotinib, or both, 3,000–5,000 BxPC-3 and MIAPaCa cells are plated per well in a 96-well plate and incubated at 37°C for the entire night. Initially, B-DIM (10-50 µM) and Erlotinib (1-5 µM) are tested at a range of concentrations. The concentrations of B-DIM (20 µM) and Erlotinib (2 µM) are selected for each assay based on the preliminary findings. The standard MTT assay is used to measure the effects of B-DIM (20 µM), Erlotinib (2 µM), and the combination on BxPC-3 and MIAPaCa cells. The assay is performed three times after 72 hours. The Tecan microplate fluorometer measures the color intensity at 595 nm. Cells treated with DMSO are given a value of 100% and are regarded as the untreated control. We have performed clonogenic assay in addition to the aforementioned assay to evaluate the effects of treatment[2].
Cell Viability Assay [2]
To test the viability of cells treated with B-DIM, Erlotinib, or the combination, BxPC-3 and MIAPaCa cells were plated (3,000–5,000 per well) in a 96-well plate and incubated overnight at 37°C. We initially tested a range of concentrations for both B-DIM (10–50 µmol/L) and erlotinib (1–5 µmol/L). Based on the initial results, the concentration of B-DIM (20 µmol/L) and erlotinib (2 µmol/L) were chosen for all assays. The effects of B-DIM (20 µmol/L), erlotinib (2 µmol/L), and the combination on BxPC-3 and MIAPaCa cells were determined by the standard 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay after 72 h and was repeated three times. The color intensity was measured by a Tecan microplate fluorometer at 595 nm. DMSO-treated cells were considered to be the untreated control and assigned a value of 100%. In addition to the above assay, we have also done clonogenic assay for assessing the effects of treatment as shown below.
Clonogenic Assay [2]
To test the survival of cells treated with B-DIM, Erlotinib, or the combination, BxPC-3 and MIAPaCa cells were plated (50,000–100,000 per well) in a six-well plate and incubated overnight at 37°C. After 72-h exposure to 20 µmol/L B-DIM, 2 µmol/L erlotinib, and the combination, the cells were trypsinized, and the viable cells were counted (trypan blue exclusion) and plated in 100 mm Petri dishes in a range of 100 to 1,000 cells to determine the plating efficiency as well as assess the effects of treatment on clonogenic survival. The cells were then incubated for ~10 to 12 days at 37°C in a 5% CO2/5% O2/90% N2 incubator. The colonies were stained with 2% crystal violet and counted. The surviving fraction was normalized to untreated control cells with respect to clonogenic efficiency, which was 83% for both BxPC-3 and MIAPaCa cells. In addition to this assay, cells were also treated similarly and plated in soft-agar (soft-agar colony assay) and incubated at 37°C. The colonies in the soft agar were also counted in all untreated and treated wells after 12 days.
Quantification of Apoptosis by ELISA [2]
The Cell Death Detection ELISA kit (Roche Applied Science) was used to detect apoptosis in untreated and treated BxPC-3 and MIAPaCa cells. Cells seeded in six-well plates were treated with B-DIM (20 µmol/L), Erlotinib (2 µmol/L), or the combination. The cells were trypsinized and ~10,000 cells were used as described earlier. Tecan microplate fluorometer was used to measure color intensity at 405 nm. The experiment was repeated three times.
Protein Extraction and Western Blot Analysis [2]
BxPC-3 and MIAPaCa cells treated with B-DIM (20 µmol/L), Erlotinib (2 µmol/L), or the combination for 72 h were used to evaluate the effects of treatment on survivin, Bcl-2, Bcl-xL, EGFR, EGFR-pTyr1173, c-IAP1/2, Src, poly(ADP-ribose) polymerase (PARP), and β-actin expression. The experiment was carried out for a minimum of three times. Cells were harvested as described previously. The samples were loaded on 7% to 12% SDSPAGE for separation and electrophoretically transferred to a nitrocellulose membrane. Each membrane was incubated with monoclonal antibody against survivin, Bcl-2, Bcl-xL, Src, c-IAP1/2, EGFR, EGFR-pTyr1173, PARP, and β-actin. Blots were incubated with secondary antibodies conjugated with peroxidase. The signal intensity was then measured using chemiluminescent detection system.
Electrophoretic Mobility Shift Assay for NF-κB Activation [2]
To evaluate the effect of B-DIM and Erlotinib on BxPC-3 and MIAPaCa cells, the cells were either untreated or treated with B-DIM (20 µmol/L), erlotinib (2 µmol/L), or the combination with a minimum repeat of experiment at least three times for 72 h. The cells or the minced tumor tissue were homogenized using a Dounce homogenizer in 400 µL ice-cold lysis buffer as described earlier.
Animal Protocol
Mice: The treatment groups consist of seven randomly assigned female ICR-SCID mice, aged 6-7 weeks: (a) control (no treatment); (b) B-DIM (50 mg/kg body weight) administered intragastrically once daily; (c) Erlotinib (50 mg/kg body weight) administered daily intraperitoneally for 15 days; and (d) B-DIM and Erlotinib administered according to the schedule for individual treatments. After receiving their last dose of medication, all mice are killed on day three, and their body weight is recorded. A portion of the tissue is immediately frozen in liquid nitrogen and kept cold (−70°C) for later use, while the remaining portion is fixed in formalin and prepared for paraffin block processing. The presence of a tumor or tumors in each pancreas is verified by staining a fixed tissue section with H&E.
Rats: Male Sprague-Dawley (SD) rats six weeks of age, weighing 180–210 g, are utilized. On day 0, SD rats (n=28) receive an intraperitoneal injection of 7 mg/kg of freshly prepared ciprofloxacin (CP) at a concentration of 1 mg/mL. For the purpose of examining Erlotinib's effects, 28 CP-N rats are split into two groups. Animals in two groups (n = 14) are given daily oral gavages of either Erlotinib (20 mg/kg) (CP+E, n = 14) or vehicle (CP+V, n = 14) from day -1 (24 hours before the CP injection) to day 3. Groups treated with vehicles are given the same amount of saline. At six weeks of age, a normal control group (NC, n = 5) consists of five male SD rats. From the first to the third day, the NC rats receive an equivalent volume of saline orally via gavage. Day 4 (96 hours post-CP injection): rats are anesthetized, and following a cardiac puncture, they are sacrificed by exsanguination. The kidneys and blood are simultaneously extracted. Renal tissue is sectioned and fixed in 2% paraformaldehyde/phosphate-buffered saline (PBS) for later use, or it can be snap-frozen in liquid nitrogen. In order to reduce suffering as much as possible, diethyl ether gas anesthesia is used during all surgical procedures.
Mice were randomized into the following treatment groups (n = 7): (a) untreated control; (b) only B-DIM (50 mg/kg body weight), intragastric once every day; (c) Erlotinib (50 mg/kg body weight), everyday i.p. for 15 days; and (d) B-DIM and Erlotinib, following schedule as for individual treatments. All mice were killed on day 3 following last dose of treatment, and their body weight was determined. One part of the tissue was rapidly frozen in liquid nitrogen and stored at −70°C for future use and the other part was fixed in formalin and processed for paraffin block. H&E staining of fixed tissue section was used to confirm the presence of tumor(s) in each pancreas. [2]
Cisplatin (CP) was freshly prepared in saline at a concentration of 1 mg ml−1 and then injected intraperitoneally in SD rats (n = 28) at a dose of 7 mg/kg on day 0. The dose of CP was selected based on a previous stud. To investigate the effect of Erlotinib, 28 CP-N rats were divided into two groups. Separate groups (n = 14) each of animals were administered with either Erlotinib (20 mg/kg, Cugai Pharmaceutical/F. Hoffmann-La Roche, Basel, Switzerland) (CP+E, n = 14) or vehicle (CP+V, n = 14) daily by oral gavage from day -1 (24 hours prior to the CP injection) to day 3. Vehicle-treated groups received an equivalent volume of saline. Five male SD rats at the age of 6 weeks were used as a normal control group (NC, n = 5). The NC rats were given an equivalent volume of saline daily by oral gavage from day -1 to day 3. At day 4 (96 hours after CP injection), each rat was anesthetized and sacrificed by exsanguination after the cardiac puncture; blood was collected by cardiac puncture and kidneys were collected (Figure 1). Renal tissue was divided; separate portions were snap-frozen in liquid nitrogen or fixed in 2% paraformaldehyde/phosphate-buffered saline (PBS) for later use. All surgery was performed under diethyl ether gas anesthesia, and all efforts were made to minimize suffering.
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
Erlotinib is about 60% absorbed after oral administration and its bioavailability is substantially increased by food to almost 100%. Peak plasma levels occur 4 hours after dosing. The solubility of erlotinib is pH dependent. Solubility decreases pH increases. Smoking also decrease the exposure of erlotinib.
Following a 100 mg oral dose, 91% of the dose was recovered in which 83% was in feces (1% of the dose as unchanged parent compound) and 8% in urine (0.3% of the dose as unchanged parent compound).
Apparent volume of distribution = 232 L
Smokers have a 24% higher rate of erlotinib clearance.
Erlotinib is about 60% absorbed after oral administration and its bioavailability is substantially increased by food to almost 100%. Peak plasma levels occur 4 hours after dosing. The solubility of erlotinib is pH dependent. Erlotinib solubility decreases as pH increases.
Following absorption, erlotinib is approximately 93% protein bound to plasma albumin and alpha-1 acid glycoprotein. Erlotinib has an apparent volume of distribution of 232 liters.
Time to reach steady state plasma concentration /is/ 7 - 8 days. No significant relationships of clearance to covariates of patient age, body weight or gender were observed. Smokers had a 24% higher rate of erlotinib clearance.
Following a 100 mg oral dose, 91% of the dose was recovered: 83% in feces (1% of the dose as intact parent) and 8% in urine (0.3% of the dose as intact parent).
For more Absorption, Distribution and Excretion (Complete) data for Erlotinib (10 total), please visit the HSDB record page.
Metabolism / Metabolites
Metabolism occurs in the liver. In vitro assays of cytochrome P450 metabolism showed that erlotinib is metabolized primarily by CYP3A4 and to a lesser extent by CYP1A2, and the extrahepatic isoform CYP1A1.
Metabolism and excretion of erlotinib, an orally active inhibitor of epidermal growth factor receptor tyrosine kinase, were studied in healthy male volunteers after a single oral dose of (14)C-erlotinib hydrochloride (100-mg free base equivalent, approximately 91 microCi/subject)... In plasma, unchanged erlotinib represented the major circulating component, with the pharmacologically active metabolite M14 accounting for approximately 5% of the total circulating radioactivity. Three major biotransformation pathways of erlotinib are O-demethylation of the side chains followed by oxidation to a carboxylic acid, M11 (29.4% of dose); oxidation of the acetylene moiety to a carboxylic acid, M6 (21.0%); and hydroxylation of the aromatic ring to M16 (9.6%). In addition, O-demethylation of M6 to M2, O-demethylation of the side chains to M13 and M14, and conjugation of the oxidative metabolites with glucuronic acid (M3, M8, and M18) and sulfuric acid (M9) play a minor role in the metabolism of erlotinib. The identified metabolites accounted for >90% of the total radioactivity recovered in urine and feces. The metabolites observed in humans were similar to those found in the toxicity species, rats and dogs.
Erlotinib has known human metabolites that include Erlotinib M14.
Biological Half-Life
Median half-life of 36.2 hours.
A population pharmacokinetic analysis in 591 patients receiving the single-agent erlotinib hydrochloride 2nd/3rd line regimen showed a median half-life of 36.2 hours.
Toxicity/Toxicokinetics
Hepatotoxicity
Elevations in serum aminotransferase levels are common during erlotinib therapy of pancreatic and lung cancers, and values above 5 times the upper limit of normal occur in at least 10% of patients. Similar rates of ALT elevations, however, can occur with comparable antineoplastic regimens. The abnormalities are usually asymptomatic and self-limited, but may require dose adjustment or discontinuation (Case 1). In addition, there have been rare reports of clinically apparent liver injury attributed to erlotinib therapy. The time to onset is typically within days or weeks of starting therapy, and the liver injury can be severe, there being at least a dozen fatal instances reported in the literature. The onset of injury can be abrupt and the pattern of serum enzyme elevations is usually hepatocellular (Case 2). Immunoallergic features (rash, fever and eosinophilia) are not common and autoantibody formation has not been reported. Routine monitoring of liver tests during therapy is recommended. The rate of clinically significant liver injury and hepatic failure is increased in patients with preexisting cirrhosis or hepatic impairment due to liver tumor burden.
Likelihood score: B (likely but uncommon cause of clinically apparent liver injury).
Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
No information is available on the clinical use of erlotinib during breastfeeding. Because erlotinib is 93% bound to plasma proteins, the amount in milk is likely to be low. However, its half-life is about 36 hours and it might accumulate in the infant. It is also given in combination with gemcitabine for pancreatic cancer, which may increase the risk to the infant. The manufacturer recommends that breastfeeding be discontinued during erlotinib therapy and for 2 weeks after the final dose.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.
Protein Binding
93% protein bound to albumin and alpha-1 acid glycoprotein (AAG)
Interactions
Because cigarette smoking reduces systemic exposure to erlotinib, patients should be advised to stop smoking. If patients continue to smoke, an increase in erlotinib dosage may be considered; upon smoking cessation, dosage of erlotinib should be reduced immediately to the starting dose level.
Drugs that increase the pH of the upper GI tract decrease the solubility of erlotinib and reduce its bioavailability.1 Concomitant administration of omeprazole, a proton pump inhibitor, decreased the area under the concentration-time curve for erlotinib by 46% and decreased the maximum concentration of erlotinib by 61%. Increasing the dose level of erlotinib is not likely to compensate for the loss of exposure, and separation of doses may not eliminate the interaction because proton pump inhibitors have an extended effect on the pH of the upper GI tract. If possible, the concomitant use of erlotinib and proton pump inhibitors should be avoided.
The use of antacids may be considered as an alternative to histamine 2 receptor blockers or proton pump inhibitors in patients receiving erlotinib. However, the effect of antacids on the disposition of erlotinib has not been studied. If use of an antacid is necessary, the antacid dose and the erlotinib dose should be separated by several hours.
Potential pharmacologic interaction (increased international normalized ratio [INR] and infrequent reports of bleeding, including GI and non-GI bleeding). Monitor prothrombin time (PT) or INR regularly in patients receiving erlotinib concomitantly with warfarin or other coumarin-derivative anticoagulants.
For more Interactions (Complete) data for Erlotinib (7 total), please visit the HSDB record page.
References

[1]. Induction of apoptosis and cell cycle arrest by CP-358,774, an inhibitor of epidermal growth factor receptor tyrosine kinase. Cancer Res. 1997, 57(21), 4838-4848.

[2]. Apoptosis-inducing effect of erlotinib is potentiated by 3,3'-diindolylmethane in vitro and in vivo using an orthotopic model of pancreatic cancer. Mol Cancer Ther, 2008, 7(6), 1708-1719.

[3]. Epidermal growth factor receptor inhibition with erlotinib partially prevents cisplatin-induced nephrotoxicity in rats. PLoS One. 2014 Nov 12;9(11):e111728.

Additional Infomation
Therapeutic Uses
Erlotinib hydrochloride monotherapy is indicated for the maintenance treatment of patients with locally advanced or metastatic non-small cell lung cancer whose disease has not progressed after four cycles of platinum-based first-line chemotherapy. /Included in US product label/
Erlotinib hydrochloride monotherapy is indicated for the treatment of patients with locally advanced or metastatic non-small cell lung cancer after failure of at least one prior chemotherapy regimen. /Included in US product label/
Erlotinib hydrochloride in combination with gemcitabine is indicated for the first-line treatment of patients with locally advanced, unresectable or metastatic pancreatic cancer. /Included in US product label/
Drug Warnings
The manufacturer states that there are no known contraindications to the use of erlotinib.
Serious, sometimes fatal, interstitial lung disease-like events have occurred in patients receiving erlotinib. Interstitial lung disease-like events have been reported in approximately 0.7% of about 4900 patients receiving erlotinib in controlled and uncontrolled studies. In the principal efficacy study for non-small cell lung cancer, the reported incidence of interstitial lung disease-like events (0.8%) was similar among patients receiving erlotinib and those receiving placebo. In the principal efficacy study for pancreatic cancer, interstitial lung disease-like events occurred in 2.5% of patients receiving erlotinib and gemcitabine versus 0.4% of those receiving placebo and gemcitabine. Onset of manifestations occurred from 5 days to more than 9 months (median: 39 days) after initiating erlotinib therapy. Reported diagnoses in patients suspected of having interstitial lung disease-like events included pneumonitis, radiation pneumonitis, hypersensitivity pneumonitis, interstitial pneumonia, interstitial lung disease, obliterative bronchiolitis, pulmonary fibrosis, acute respiratory distress syndrome, and lung infiltration. Among patients receiving erlotinib for non-small cell lung cancer, most of these cases were associated with confounding or contributing factors, including concomitant or prior chemotherapy, prior radiotherapy, preexisting parenchymal lung disease, metastatic lung disease, or pulmonary infections.
Interruption or discontinuance of erlotinib therapy may be required in patients experiencing pulmonary toxicity.
Hepatorenal syndrome or acute renal failure, sometimes fatal, and renal insufficiency, with or without hypokalemia, have been reported in patients receiving erlotinib. Factors contributing to these adverse renal effects included baseline hepatic impairment; severe dehydration caused by diarrhea, vomiting, and/or anorexia; and concurrent chemotherapy. If dehydration occurs, erlotinib therapy should be interrupted and rehydration measures should be initiated. Periodic monitoring of renal function and serum electrolytes is recommended in patients at risk of dehydration.
For more Drug Warnings (Complete) data for Erlotinib (27 total), please visit the HSDB record page.
The epidermal growth factor receptor (EGFR) is overexpressed in a significant percentage of carcinomas and contributes to the malignant phenotype. CP-358,774 is a directly acting inhibitor of human EGFR tyrosine kinase with an IC50 of 2 nM and reduces EGFR autophosphorylation in intact tumor cells with an IC50 of 20 nM. This inhibition is selective for EGFR tyrosine kinase relative to other tyrosine kinases we have examined, both in assays of isolated kinases and whole cells. At doses of 100 mg/kg, CP-358,774 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. CP-358,774 inhibits the proliferation of DiFi human colon tumor cells at submicromolar concentrations in cell culture and blocks cell cycle progression at the G1 phase. This inhibitor produces a marked accumulation of retinoblastoma protein in its underphosphorylated form and accumulation of p27KIP1 in DiFi cells, which may contribute to the cell cycle block. Inhibition of the EGFR also triggers apoptosis in these cells as determined by formation of DNA fragments and other criteria. These results indicate that CP-358,774 has potential for the treatment of tumors that are dependent on the EGFR pathway for proliferation or survival. [1]
Blockade of epidermal growth factor receptor (EGFR) by EGFR tyrosine kinase inhibitors is insufficient for effective antitumor activity because of independently activated survival pathways. A multitargeted approach may therefore improve the outcome of anti-EGFR therapies. In the present study, we determined the effects of 3,3'-diindolylmethane (Bioresponse BR-DIM referred to as B-DIM), a formulated DIM with greater bioavailability on cell viability and apoptosis with erlotinib in vitro and in vivo using an orthotopic animal tumor model. BxPC-3 and MIAPaCa cells with varying levels of EGFR and nuclear factor-kappaB (NF-kappaB) DNA-binding activity were treated with B-DIM (20 micromol/L), erlotinib (2 micromol/L), and the combination. Cell survival and apoptosis was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and histone-DNA ELISA. Electrophoretic mobility shift assay was used to evaluate NF-kappaB DNA-binding activity. We found significant reduction in cell viability by both 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and clonogenic assays, induction of apoptosis, down-regulation of EGFR phosphorylation, NF-kappaB DNA-binding activity, and expression of antiapoptotic genes in BxPC-3 cells when treated with the combination of erlotinib and B-DIM compared with either agent alone. In contrast, no such effect was observed in MIAPaCa cells by similar treatment. Most importantly, these in vitro results were recapitulated in animal model showing that B-DIM in combination with erlotinib was much more effective as an antitumor agent compared with either agent alone. These results suggest that the utilization of B-DIM could be a useful strategy for achieving better treatment outcome in patients with activated status of EGFR and NF-kappaB in their tumors. [2]
With respect to limitations of this study, we must consider several issues. First, food intake was not controlled among the three groups. Since the animals were not pair fed, it was hard to determine whether BW loss was depending on low intake or influence of CP induced AKI itself. Second, the present study did not address tubular dysfunction including salt and magnesium wasting, which is one of the most common physiological abnormalities associated with CP-N. Third, the therapeutic effect of erlotinib on recovery phase from CP-induced AKI was not investigated. Clinically, therapeutic effect on recovery phase as well as preventive effect on early phase is thought to be relevant to patients receiving CP chemotherapy. Lastly, the influence of erlotinib on antitumorigenic effects of CP was not proved. Further studies to evaluate whether the reduction of CP-elicited cell death by erlotinib was specific for the kidney by using different tumor cell lines like previous studies are needed.
In conclusion, our in vivo and in vitro studies show that erlotinib has a renoprotective effect in CP-N, an effect that might be attributable to the attenuation of the apoptosis and proliferation of proximal tubular cells. Protection by erlotinib appears to be mediated through the inhibition of downstream signaling of EGFR, including MAPK and PI3K-Akt. These results suggest that erlotinib may be useful for preventing AKI in patients receiving CP chemotherapy.[3]
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C22H23N3O4
Molecular Weight
393.44
Exact Mass
393.168
Elemental Analysis
C, 67.16; H, 5.89; N, 10.68; O, 16.27
CAS #
183321-74-6
Related CAS #
Erlotinib Hydrochloride;183319-69-9;Erlotinib mesylate;248594-19-6;Erlotinib-d6;1034651-23-4;Erlotinib-13C6;1211107-68-4
PubChem CID
176870
Appearance
White to off-white crystalline powder
Density
1.2±0.1 g/cm3
Boiling Point
553.6±50.0 °C at 760 mmHg
Melting Point
223 - 228ºC
Flash Point
288.6±30.1 °C
Vapour Pressure
0.0±1.5 mmHg at 25°C
Index of Refraction
1.615
LogP
2.39
Hydrogen Bond Donor Count
1
Hydrogen Bond Acceptor Count
7
Rotatable Bond Count
11
Heavy Atom Count
29
Complexity
525
Defined Atom Stereocenter Count
0
SMILES
O(C([H])([H])C([H])([H])OC([H])([H])[H])C1C([H])=C2C(=NC([H])=NC2=C([H])C=1OC([H])([H])C([H])([H])OC([H])([H])[H])N([H])C1=C([H])C([H])=C([H])C(C#C[H])=C1[H]
InChi Key
AAKJLRGGTJKAMG-UHFFFAOYSA-N
InChi Code
InChI=1S/C22H23N3O4/c1-4-16-6-5-7-17(12-16)25-22-18-13-20(28-10-8-26-2)21(29-11-9-27-3)14-19(18)23-15-24-22/h1,5-7,12-15H,8-11H2,2-3H3,(H,23,24,25)
Chemical Name
N-(3-ethynylphenyl)-6,7-bis(2-methoxyethoxy)quinazolin-4-amine
Synonyms
Erlotinib free base; NSC718781; NSC718781; CP358774; OSI-774; OSI 774; NSC 718781; CP-358,774; CP-358774; OSI774
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO: ~4.0 mg/mL
Water: <1 mg/mL
Ethanol: ~15 mg/mL(~38.1 mM)
Solubility (In Vivo)
Solubility in Formulation 1: 10 mg/mL (25.42 mM) in 50% PEG300 + 50% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: 10 mg/mL (25.42 mM) in 0.5% CMC-Na/saline water (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 2.5417 mL 12.7084 mL 25.4168 mL
5 mM 0.5083 mL 2.5417 mL 5.0834 mL
10 mM 0.2542 mL 1.2708 mL 2.5417 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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Clinical Trial Information
Testing of Bevacizumab, Erlotinib, and Atezolizumab in Combination for Advanced-Stage Kidney Cancer
CTID: NCT04981509
Phase: Phase 2    Status: Recruiting
Date: 2024-12-02
Genetic Testing in Screening Patients With Stage IB-IIIA Non-small Cell Lung Cancer That Has Been or Will Be Removed by Surgery (The ALCHEMIST Screening Trial)
CTID: NCT02194738
Phase: N/A    Status: Recruiting
Date: 2024-12-02
Erlotinib in Combination With Select Tyrosine Kinase Inhibitors in Adult Patients With Advanced Solid Tumors
CTID: NCT06161558
Phase: Phase 1    Status: Not yet recruiting
Date: 2024-12-02
A Study of ASP2215 in Combination With Erlotinib in Subjects With Epidermal Growth Factor Receptor (EGFR) Activating Mutation-Positive (EGFRm+) Advanced Non-Small-Cell Lung Cancer (NSCLC) Who Have Acquired Resistance to an EGFR Tyrosine Kinase Inhibitor (TKI)
CTID: NCT02495233
Phase: Phase 1/Phase 2    Status: Terminated
Date: 2024-11-27
A Study of LY2875358 in Participants With Non-Small Cell Lung Cancer With Activating Epidermal Growth Factor Receptor Mutations
CTID: NCT01897480
Phase: Phase 2    Status: Active, not recruiting
Date: 2024-11-27
View More

Erlotinib, Gemcitabine and Nab-Paclitaxel in Advanced Pancreatic Cancer
CTID: NCT01010945
Phase: Phase 1    Status: Completed
Date: 2024-11-21


A Rollover Study for Subjects That Have Participated in an Astellas Sponsored Linsitinib Trial
CTID: NCT02057380
Phase: Phase 2    Status: Completed
Date: 2024-11-20
Phase 2 Study of Maintenance OSI-906 Plus Erlotinib (Tarceva®), or Placebo Plus Erlotinib in Patients With Nonprogression Following 4 Cycles of Platinum-based Chemotherapy
CTID: NCT01186861
Phase: Phase 2    Status: Completed
Date: 2024-11-20
Study of Erlotinib (Tarceva®) in Combination With OSI-906 in Patients With Advanced Non-small Cell Lung Cancer (NSCLC) With Activating Mutations of the Epidermal Growth Factor Receptor (EGFR) Gene
CTID: NCT01221077
Phase: Phase 2    Status: Completed
Date: 2024-11-20
A Phase 1 Dose-escalation Study of OSI-906 and Erlotinib (Tarceva®)
CTID: NCT00739453
Phase: Phase 1    Status: Completed
Date: 2024-11-20
Basal-like PDAC Treated With Gemcitabine, Erlotinib, and Nab-paclitaxel
CTID: NCT06483555
Phase: Phase 1/Phase 2    Status: Not yet recruiting
Date: 2024-11-15
Early Prediction of Therapeutic Response to Targeted Therapy in Stage IIIB/IV or Recurrent Lung Cancer Patients
CTID: NCT00708448
Phase: Phase 1    Status: Completed
Date: 2024-11-14
Canadian Profiling and Targeted Agent Utilization Trial (CAPTUR)
CTID: NCT03297606
Phase: Phase 2    Status: Recruiting
Date: 2024-11-12
KPMNG Study of MOlecular Profiling Guided Therapy Based on Genomic Alterations in Advanced Solid Tumors II
CTID: NCT05525858
Phase:    Status: Recruiting
Date: 2024-11-12
A Study to Evaluate the Safety, Pharmacokinetics, and Activity of GDC-6036 Alone or in Combination in Participants With Advanced or Metastatic Solid Tumors With a KRAS G12C Mutation
CTID: NCT04449874
Phase: Phase 1    Status: Recruiting
Date: 2024-11-05
A Study of Abemaciclib (LY2835219) in Participants With Previously Treated KRAS Mutated Lung Cancer
CTID: NCT02152631
Phase: Phase 3    Status: Active, not recruiting
Date: 2024-10-21
A Phase I, Open-Label, Multi-center Study to Assess the Safety, Tolerability and Pharmacokinetics of AZD6244 (ARRY-142886)
CTID: NCT00600496
Phase: Phase 1    Status: Active, not recruiting
Date: 2024-10-16
First Line Treatment in EGFR Mutation Positive Advanced NSCLC Patients with Central Nervous System (CNS) Metastases
CTID: NCT03653546
Phase: Phase 2/Phase 3    Status: Completed
Date: 2024-10-15
Study of the CHK1 Inhibitor BBI-355, an EcDNA-directed Therapy (ecDTx), in Subjects with Tumors with Oncogene Amplifications
CTID: NCT05827614
Phase: Phase 1    Status: Recruiting
Date: 2024-10-08
Study of Chemotherapy with Cisplatin/Carboplatin, and Docetaxel with or Without Erlotinib in Patients with Head and Neck Squamous Cell Carcinomas Amenable for Surgical Resection
CTID: NCT01927744
Phase: Phase 2    Status: Recruiting
Date: 2024-10-03
Molecular Profiling and Targeted Therapy for Advanced Non-Small Cell Lung Cancer, Small Cell Lung Cancer, and Thymic Malignancies
CTID: NCT01306045
Phase: Phase 2    Status: Completed
Date: 2024-10-01
A Study to Learn About the Effectiveness of Cancer Medicines in Patients With Metastatic Non-small Cell Lung Cancer in Norway.
CTID: NCT05834348
Phase:    Status: Completed
Date: 2024-09-04
A Study of Ramucirumab (LY3009806) in Combination With Erlotinib in Previously Untreated Participants With EGFR Mutation-Positive Metastatic NSCLC (RELAY)
CTID: NCT02411448
Phase: Phase 3    Status: Active, not recruiting
Date: 2024-08-29
AZD9291 Versus Gefitinib or Erlotinib in Patients With Locally Advanced or Metastatic Non-small Cell Lung Cancer
CTID: NCT02296125
Phase: Phase 3    Status: Active, not recruiting
Date: 2024-08-21
Epidermal Growth Factor Receptor Inhibition for Keratinopathies
CTID: NCT06545695
Phase: Phase 1/Phase 2    Status: Not yet recruiting
Date: 2024-08-09
Safety of MP470 in Combination With Standard-of-Care Chemotherapy Regimens to Treat Solid Tumors
CTID: NCT00881166
Phase: Phase 1    Status: Completed
Date: 2024-08-02
A Global Study to Assess the Effects of MEDI4736 (Durvalumab), Given as Monotherapy or in Combination With Tremelimumab Determined by PD-L1 Expression Versus Standard of Care in Patients With Locally Advanced or Metastatic Non Small Cell Lung Cancer
CTID: NCT02352948
Phase: Phase 3    Status: Completed
Date: 2024-07-26
My Pathway: A Study Evaluating Herceptin/Perjeta, Tarceva, Zelboraf/Cotellic, Erivedge, Alecensa, and Tecentriq Treatment Targeted Against Certain Molecular Alterations in Participants With Advanced Solid Tumors
CTID: NCT02091141
Phase: Phase 2    Status: Completed
Date: 2024-07-23
Docetaxel, Cisplatin, and Erlotinib Hydrochloride in Treating Patients With Stage I-III Non-small Cell Lung Cancer Following Surgery
CTID: NCT00254384
Phase: Phase 1    Status: Completed
Date: 2024-07-05
OSI-774/Cisplatin/Taxotere in Head & Neck Squamous Cell Cancer
CTID: NCT00076310
Phase: Phase 2    Status: Active, not recruiting
Date: 2024-07-05
A Study Evaluating the Safety, Pharmacokinetics (PK), and Preliminary Efficacy of ABBV-399 in Participants With Advanced Solid Tumors
CTID: NCT02099058
Phase: Phase 1    Status: Active, not recruiting
Date: 2024-06-18
A Phase II Randomized Study Comparing the Efficacy and Safety of Targeted Therapy or Cancer Immunotherapy Versus Platinum-Based Chemotherapy in Patients With Cancer of Unknown Primary Site
CTID: NCT03498521
Phase: Phase 2    Status: Active, not recruiting
Date: 2024-06-14
Study of IRX4204 With Erlotinib in Previously Treated Advanced NSCLC
CTID: NCT02991651
Phase: Phase 1    Status: Suspended
Date: 2024-04-03
A Phase 1/2 Trial of Trametinib and Erlotinib in Patients With EGFR-Mutant Lung Adenocarcinomas and Acquired Resistance to Erlotinib
CTID: NCT03076164
Phase: Phase 1/Phase 2    Status: Completed
Date: 2024-04-02
Erlotinib Hydrochloride in Preventing Liver Cancer in Patients With Cirrhosis of the Liver
CTID: NCT02273362
Phase: Phase 1/Phase 2    Status: Completed
Date: 2024-03-26
Serial Measurements of Molecular and Architectural Responses to Therapy (SMMART) PRIME Trial
CTID: NCT03878524
Phase: Phase 1    Status: Terminated
Date: 2024-03-04
A Phase II Study of Bevacizumab and Erlotinib in Subjects With Advanced Hereditary Leiomyomatosis and Renal Cell Cancer (HLRCC) or Sporadic Papillary Renal Cell Cancer
CTID: NCT01130519
Phase: Phase 2    Status: Active, not recruiting
Date: 2024-02-01
The Drug Rediscovery Protocol (DRUP Trial)
CTID: NCT02925234
Phase: Phase 2    Status: Recruiting
Date: 2024-01-24
Erlotinib and RAD001 (Everolimus) in Patients With Previously Treated Advanced Pancreatic Cancer
CTID: NCT00640978
Phase: Phase 2    Status: Terminated
Date: 2023-10-18
Erlotinib (Tarceva) and Bexarotene (Targretin) Oral Capsules in Advanced Cancers of the Aerodigestive Tract
CTID: NCT01116622
Phase: Phase 1    Status: Completed
Date: 2023-10-18
Trial of RAD001 and Erlotinib With Recurrent Head and Neck Squamous Cell Carcinoma
CTID: NCT00942734
Phase: Phase 2    Status: Completed
Date: 2023-10-18
Pilot Study of Erlotinib for the Treatment of Patients With de Novo Acute Myeloid Leukemia
CTID: NCT01174043
Phase: Phase 2    Status: Completed
Date: 2023-10-13
Brazilian Lung Immunotherapy Study
CTID: NCT05081674
Phase: Phase 2    Status: Completed
Date: 2023-10-11
The Rome Trial From Histology to Target: the Road to Personalize Target Therapy and Immunotherapy
CTID: NCT04591431
Phase: Phase 2    Status: Active, not recruiting
Date: 2023-10-03
To Evaluate OBI-833/OBI-821 in Combination With First-Line Erlotinib in Patients With EGFR-Mutated, Globo H-Positive, Locally Advanced or Metastatic Non-Small Cell Lung Cancer
CTID: NCT05442060
Phase: Phase 2    Status: Recruiting
Date: 2023-08-07
A Phase 2 Exploratory Study of Erlotinib and SNDX-275 in Participants With Non-small Cell Lung Carcinoma Who Are Progressing on Erlotinib
CTID: NCT00750698
Phase: Phase 2    Status: Terminated
Date: 2023-07-06
Eribulin Mesylate in Combination With Intermittent Erlotinib in Patients With Previously Treated, Advanced Non-Small Cell Lung Cancer
CTID: NCT01104155
Phase: Phase 2    Status: Completed
Date: 2023-06-22
A Phase II Stydy of Bevacizumab Plus Erlotinib in Patients for Krebs Cycle Altered Cancer
CTID: NCT05904457
Phase: Phase 2    Status: Recruiting
Date: 2023-06-15
The Study Observes How Long Patients With Non-small Cell Lung Cancer (NSCLC) Benefit From Treatment With Epidermal Growth Factor Tyrosine Kinase Inhibitor (EGFR-TKI) When Given Either for Uncommon Mutations or for Common Mutations in the Sequence Afatinib Followed by Osimertinib
CTID: NCT04179890
Phase:    Status: Completed
Date: 2023-05-25
EGFR Inhibition Using Weekly Erlotinib for Recurrent Malignant Gliomas
CTID: NCT01257594
Phase: Phase 1    Status: Completed
Date: 2023-05-25
Phase II Open-Label Trial of Tarceva in Women With Metastatic, Hormone- and HER2-Negative Breast Cancer
CTID: NCT00597597
Phase: Phase 2    Status: Terminated
Date: 2023-05-17
Study of Ixazomib and Erlotinib in Solid Tumors
CTID: NCT02942095
Phase: Phase 1    Status: Completed
Date: 2023-04-18
Study of TARCEVA (Erlotinib) as Adjuvant Treatment for Locally Advanced Head and Neck Squamous Cell Carcinoma
CTID: NCT01515137
Phase: Phase 1    Status: Completed
Date: 2023-03-28
Study Comparing Bevacizumab + Erlotinib vs Erlotinib Alone as First Line Treatment of Patients With EGFR Mutated Advanced Non Squamous Non Small Cell Lung Cancer
CTID: NCT02633189
Phase: Phase 3    Status: Active, not recruiting
Date: 2023-03-24
A Phase I/IB Trial of MEK162 in Combination With Erlotinib in NSCLC Harboring KRAS or EGFR Mutation
CTID: NCT01859026
Phase: Phase 1    Status: Completed
Date: 2023-01-19
A Study of Pembrolizumab (MK-3475) in Combination With Chemotherapy or Immunotherapy in Participants With Non-small Cell Lung Cancer (MK-3475-021/KEYNOTE-021)
CTID: NCT02039674
Phase: Phase 1/Phase 2    Status: Completed
Date: 2022-11-08
Erlotinib Plus Bevacizumab in Hepatocellular Carcinoma (HCC) as Second-line Therapy
CTID: NCT01180959
Phase: Phase 2    Status: Completed
Date: 2022-11-07
ProTarget - A Danish Nationwide Clinical Trial on Targeted Cancer Treatment Based on Genomic Profiling
CTID: NCT04341181
Phase: Phase 2    Status: Recruiting
Date: 2022-10-26
Testing of Drugs Erlotinib and Docetaxel in Lung Cancer Patients Classified Regarding Their Outlook Using VeriStrat®.
CTID: NCT01652469
Phase: Phase 3    Status: Completed
Date: 2022-08-24
BELIEF (Bevacizumab and ErLotinib In EGFR Mut+ NSCLC)
CTID: NCT01562028
Phase: Phase 2    Status: Completed
Date: 2022-08-24
Study to Evaluate Erlotinib With or Without SNDX-275 (Entinostat) in the Treatment of Patients With Advanced NSCLC
CTID: NCT00602030
Phase: Phase 1/Phase 2    Status: Completed
Date: 2022-08-22
A Study of BGB324(Bemcentinib) in Combination With Erlotinib in Patients With Non-Small Cell Lung Cancer
CTID: NCT02424617
Phase: Phase 1/Phase 2    Status: Completed
Date: 2022-08-18
Erlotinib Hydrochloride in Reducing Duodenal Polyp Burden in Patients With Familial Adenomatous Polyposis at Risk of Developing Colon Cancer
CTID: NCT02961374
Phase: Phase 2    Status: Completed
Date: 2022-07-26
Study of Bevacizumab and Erlotinib in Patients With Advanced Non-small Cell Lung Cancer
CTID: NCT00553800
Phase: Phase 2    Status: Completed
Date: 2022-07-12
Pemetrexed in Combination With Erlotinib as a Salvage Treatment in Patients With Metastatic Biliary Tract Cancer (BTC) Who Failed Gemcitabine Containing Chemotherapy: A Phase II Single Arm Prospective Study
CTID: NCT03110484
Phase: Phase 2    Status: Unknown status
Date: 2022-06-15
Pemetrexed Plus Tarceva as Salvage Treatment in EGFR Overexpressed Metastatic Colorectal Cancer Patients Who Were Failed After Standard Chemotherapy
CTID: NCT03086538
Phase: Phase 2    Status: Completed
Date: 2022-06-15
Individualized Treatment Based on Epidermal Growth Factor Receptor Mutations and Level of BRCA1 Expression in Advanced Adenocarcinoma
CTID: NCT00883480
Phase: N/A    Status: Completed
Date: 2022-06-13
Phase III Study (Tarceva®) vs Chemotherapy to Treat Advanced Non-Small Cell Lung Cancer in Patients With Mutations in the TK Domain of EGFR
CTID: NCT00446225
Phase: Phase 3    Status: Completed
Date: 2022-06-13
KD019 Versus Erlotinib in Subjects With Stage IIIB/IV Non Small Cell Lung Cancer With Progression After First- or Second-Line Chemotherapy
CTID: NCT01487174
Phase: Phase 3    Status: Terminated
Date: 2022-05-13
Neoadjuvant Erlotinib for Operable Stage II or IIIA NSCLC With EGFR Mutations
CTID: NCT01470716
Phase: Phase 2    Status: Unknown status
Date: 2022-04-06
A Study of Tarceva vs. Avastin+Tarceva for Advanced NSCLC With EGFR m(+)
CTID: NCT03126799
Phase: Phase 2    Status: Unknown status
Date: 2022-04-06
Sorafenib/Erlotinib Versus Erlotinib Alone in Previously Treated Advanced Non-Small-Cell Lung Cancer (NSCLC)
CTID: NCT00600015
Phase: Phase 2    Status: Completed
Date: 2022-03-10
Efficacy and Safety of Precision Therapy in Refractory Tumor
CTID: NCT03239015
Phase: Phase 2    Status: Unknown status
Date: 2022-03-04
Chemotherapy, Radiation Therapy and Immunotherapy Prior to Surgery in Operable Esophageal Cancer
CTID: NCT00393068
Phase: Phase 2    Status: Completed
Date: 2022-03-02
TUSC2-nanoparticles and Erlotinib in Stage IV Lung Cancer
CTID: NCT01455389
Phase: Phase 1/Phase 2    Status: Terminated
Date: 2022-03-02
BATTLE-2 Program: A Biomarker-Integrated Targeted Therapy Study in Previously Treated Patients With Advanced Non-Small Cell Lung Cancer
CTID: NCT01248247
Phase: Phase 2    Status: Completed
Date: 2022-01-12
A Study of LY3499446 in Participants With Advanced Solid Tumors With KRAS G12C Mutation
CTID: NCT04165031
Phase: Phase 1/Phase 2    Status: Terminated
Date: 2021-11-24
Study to Assess Food Effect on Pharmacokinetics of Entinostat in Subjects With Breast Cancer or Non-Small Cell Lung Cancer
CTID: NCT01594398
Phase: Phase 1    Status: Completed
Date: 2021-11-19
Study of Nivolumab (BMS-936558) in Combination With Gemcitabine/Cisplatin, Pemetrexed/Cisplatin, Carboplatin/Paclitaxel, Bevacizumab Maintenance, Erlotinib, Ipilimumab or as Monotherapy in Subjects With Stage IIIB/IV Non-small Cell Lung Cancer (NSCLC) (CheckMate 012)
CTID: NCT01454102
Phase: Phase 1    Status: Completed
Date: 2021-10-12
Study of Erlotinib and Chemotherapy for Unresectable or Metastatic Cancer of the Esophagus and Gastric Cardia
CTID: NCT00591123
Phase: Phase 2    Status: Completed
Date: 2021-10-01
Tarceva With Whole Brain Radiation Therapy - Brain Mets From Non-Small Cell Lung Cancer
CTID: NCT00871923
Phase: Phase 2    Status: Completed
Date: 2021-09-16
Phase I / II Vorinostat, Erlotinib and Temozolomide for Recurrent Glioblastoma Multiforme (GBM)
CTID: NCT01110876
Phase: Phase 1/Phase 2    Status: Terminated
Date: 2021-08-25
Study of Erlotinib With or Without Investigational Drug (U3-1287) in Subjects With Advanced Non-small Cell Lung Cancer
CTID: NCT01211483
Phase: Phase 1/Phase 2    Status: Completed
Date: 2021-06-16
A Study of Enzastaurin and Erlotinib in Participants With Solid Tumors and Lung Cancer
CTID: NCT00452413
Phase: Phase 1/Phase 2    Status: Completed
Date: 2021-05-13
CS-7017 in Combination With Erlotinib in Subjects With Stage IIIb/IV Non-small Cell Lung Cancer (NSCLC)
CTID: NCT01199068
Phase: Phase 1    Status: Completed
Date: 2021-05-13
A Study of Nivolumab in Advanced Non-Small Cell Lung Cancer (NSCLC)
CTID: NCT02574078
Phase: Phase 1/Phase 2    Status: Completed
Date: 2021-05-06
Metformin Combined With Chemotherapy for Pancreatic Cancer
CTID: NCT01210911
Phase: Phase 2    Status: Completed
Date: 2021-04-21
Determination of Intratumoral Concentrations of Kinase Inhibitors in Patients With Advanced Solid Malignancies.
CTID: NCT01636908
Phase: N/A    Status: Completed
Date: 2021-04-15
Tivantinib Plus Erlotinib Versus Placebo Plus Erlotinib for the Treatment of Non-squamous, Non-small-cell Lung Cancer
CTID: NCT01244191
Phase: Phase 3    Status: Terminated
Date: 2021-04-06
Thoracal Radiotherapy and Tarceva
CTID: NCT02714530
Phase: Phase 2    Status: Terminated
Date: 2021-03-30
Randomized, Double Blind Multicenter Phase II Study of Time to Progression on Fulvestrant in Combination With Erlotinib or Placebo in Hormone Receptor-Positive Metastatic Breast Cancer (MBC) Subjects Who Progressed on First Line Hormonal Therapy
CTID: NCT00570258
Phase: Phase 2    Status: Terminated
Date: 2021-03-30
Study of Pralatrexate vs. Erlotinib for Non-Small Cell Lung Cancer After at Least 1 Prior Platinum-based Treatment
CTID: NCT00606502
Phase: Phase 2    Status: Completed
Date: 2021-03-05
Gemcitabine and Pulse Dose Erlotinib in Second Line Treatment of Advanced Pancreatic Cancer
CTID: NCT02154737
Phase: Phase 1    Status: Completed
Date: 2021-03-02
Hormone Receptor Positive Disease Across Solid Tumor Types: A Phase I Study of Single-Agent Hormone Blockade and Combination Approaches With Targeted Agents to Provide Synergy and Overcome Resistance
CTID: NCT01197170
Phase: Phase 1    Status: Completed
Date: 2021-01-22
Stereotactic Radiosurgery or Other Local Ablation Then Erlotinib in Epidermal Growth Factor Receptor (EGFR)
CTID: NCT01573702
Phase: Phase 2    Status: Completed
Date: 2021-01-12
Lung Cancer in Women Treated With Anti-oestrogens anD Inhibitors of EGFR
CTID: NCT01556191
Phase: Phase 2    Status: Completed
Date: 2021-01-08
A Study of the Effect of R1507 in Combination With Tarceva (Erlotinib) on Progression-Free Survival in Patients With Stage IIIb/IV Non-Small Cell Lung Cancer (NSCLC).
CTID: NCT00760929
Phase: Phase 2    Status: Terminated
Date: 2021-01-05
Combination of RAD001 and Erlotinib in Patients With Advanced Non Small Cell Lung Cancer Previously Treated Only With Chemotherapy
CTID: NCT00456833
Phase: Phase 1    Status: Completed
Date: 2020-12-21
Tarceva And Radiotherapy in Locally Advanced Lung Cancer Non-small Cell Lung Cancer
CTID: NCT00888511
Phase: Phase 2    Status: Completed
Date: 2020-11-27
A Phase 2, Study of Ficlatuzumab Plus Erlotinib vs. Placebo Plus Erlotinib in Subjects With Previously Untreated Metastatic, EGFR-mutated NSCLC and BDX004 Positive Label
CTID: NCT02318368
Phase: Phase 2    Status: Terminated
Date: 2020-10-22
Bevacizumab Plus EGFR-TKIs in Chinese Patients With EGFR-mutant NSCLC: a Real-world Study
CTID: NCT04575415
Phase:    Status: Unknown status
Date: 2020-10-20
HGG-TCP (High Grade Glioma - Tumor Concentrations of Protein Kinase Inhibitors)
CTID: NCT02239952
Phase: N/A    Status: Unknown status
Date: 2020-10-08
Erlotinib Hydrochloride With or Without Bevacizumab in Treating Patients With Stage IV Non-small Cell Lung Cancer With Epidermal Growth Factor Receptor Mutations
CTID: NCT01532089
Phase: Phase 2    Status: Completed
Date: 2020-10-06
2nd Line Erlotinib Treatment With (Out) Chemotherapy of Advanced Non Small Cell Lung Cancer (NSCLC)
CTID: NCT00835471
Phase: Phase 2    Status: Completed
Date: 2020-09-29
RAD001 and Erlotinib in Patients With Neuroendocrine Tumors
CTID: NCT00843531
Phase: Phase 2    Status: Terminated
Date: 2020-09-29
MK-0646 and Gemcitabine +/- Erlotinib for Patients With Advanced Pancreatic Cancer
CTID: NCT00769483
Phase: Phase 1/Phase 2    Status: Completed
Date: 2020-09-03
Cabozantinib and Erlotinib for Patients With EGFR and c-Met Co-expressing Metastatic Pancreatic Adenocarcinoma
CTID: NCT03213626
Phase: Phase 2    Status: Terminated
Date: 2020-08-27
Trial of Erlotinib in Patients With JAK-2 V617F Positive Polycythemia Vera
CTID: NCT01038856
Phase: Phase 2    Status: Terminated
Date: 2020-08-24
Erlotinib and SBRT in Treating Patients With Locally Advanced or Metastatic Non-Small Cell Lung Cancer
CTID: NCT00547105
Phase: Phase 2    Status: Completed
Date: 2020-08-21
Erlotinib and Sirolimus in Treating Patients With Recurrent Malignant Glioma
CTID: NCT00509431
Phase: Phase 1    Status: Completed
Date: 2020-07-31
Erlotinib, Paclitaxel, and Carboplatin Combined With Radiation Therapy for Stage III Non-Small Cell Lung Cancer
CTID: NCT00278148
Phase: Phase 1/Phase 2    Status: Completed
Date: 2020-07-20
Erlotinib With or Without Hydroxychloroquine in Chemo-Naive Advanced NSCLC and (EGFR) Mutations
CTID: NCT00977470
Phase: Phase 2    Status: Unknown status
Date: 2020-07-14
Almonertinib Vs. Erlotinib/Chemotherapy for Neo-adjuVant Treatment of Stage IIIA-N2 EGFR-mutated NSCLC
CTID: NCT04455594
Phase: Phase 2    Status: Not yet recruiting
Date: 2020-07-02
Bevacizumab in Multiple Phase I Combinations
CTID: NCT00543504
Phase: Phase 1    Status: Completed
Date: 2020-06-30
Study of Erlotinib With or Without Investigational Drug (CS-7017) in Subjects With Advanced Non-small Cell Lung Cancer
CTID: NCT01101334
Phase: Phase 2    Status: Completed
Date: 2020-06-16
Erlotinib in Treating Patients With Recurrent or Metastatic Skin Squamous Cell Carcinoma
CTID: NCT01198028
Phase: Phase 2    Status: Completed
Date: 2020-06-11
Carbon Ion Radiation Therapy for Locally Advanced Pancreatic Cancer
CTID: NCT03403049
Phase: Phase 1    Status: Completed
Date: 2020-04-22
Erlotinib Prevention of Oral Cancer (EPOC)
CTID: NCT00402779
Phase: Phase 3    Status: Completed
Date: 2020-04-21
Phase I Study of a Statin + Erlotinib for Advanced Solid Malignancies With Focus on Squamous Cell Carcinomas and NSCLC
CTID: NCT00966472
Phase: Phase 1    Status: Completed
Date: 2020-04-21
A Phase 1b Study of Atezolizumab in Combination With Erlotinib or Alectinib in Participants With Non-Small Cell Lung Cancer (NSCLC)
CTID: NCT02013219
Phase: Phase 1    Status: Completed
Date: 2020-04-21
Study of OSI-774 (Tarceva) in Previously Untreated Elderly Lung Cancer Patients
CTID: NCT00137800
Phase: Phase 2    Status: Completed
Date: 2020-04-03
Chemotherapy & Erlotinib in Treating Patients w/ Esophageal or Gastroesophageal Cancer That Cannot Be Removed by Surgery
CTID: NCT00539617
Phase: Phase 2    Status: Terminated
Date: 2020-03-23
Genomics-Based Target Therapy for Children With Relapsed or Refractory Malignancy
CTID: NCT02638428
Phase: Phase 2    Status: Unknown status
Date: 2020-03-19
Randomized Comparative Study of Erlotinib and Pemetrexed in the Maintenance Treatment of Advanced Lung Cancer Patients.
CTID: NCT03460678
Phase: Phase 4    Status: Terminated
Date: 2020-03-05
A Safety and Efficacy Study of INC280 Alone, and in Combination With Erlotinib, Compared to Chemotherapy, in Advanced/Metastatic Non-small Cell Lung Cancer Patients With EGFR Mutation and cMET Amplification
CTID: NCT02468661
Phase: Phase 1    Status: Terminated
Date: 2020-02-24
BATTLE Program: Tarceva and Targretin in Patients With Advanced Non-Small Cell Lung Cancer (NSCLC)
CTID: NCT00411632
Phase: Phase 2    Status: Completed
Date: 2020-01-29
Pemetrexed and Erlotinib for Metastatic Colorectal Cancer
CTID: NCT02723578
Phase: Phase 2    Status: Completed
Date: 2020-01-13
OSI-774 (Erlotinib, Tarceva) in Elderly Patients
CTID: NCT00200395
Phase: Phase 2    Status: Completed
Date: 2019-12-30
A Study of Erlotinib in Participants With Locally Advanced or Metastatic Non-Small Cell Lung Cancer
CTID: NCT01667562
Phase: Phase 3    Status: Completed
Date: 2019-12-20
Erlotinib in Women With Previously Untreated Adenocarcinoma of the Lung
CTID: NCT00137839
Phase: Phase 2    Status: Completed
Date: 2019-12-17
The Role of Erlotinib an Epidermal Growth Factor Receptor (EGFR) Inhibitor in the Treatment of Myelodysplastic Syndrome
CTID: NCT00570375
Phase: Phase 2    Status: Withdrawn
Date: 2019-11-25
Phase II Study Of Neoadjuvant Chemotherapy In Borderline Resectable Pancreatic Adenocarcinoma
CTID: NCT00728000
Phase: Phase 2    Status: Withdrawn
Date: 2019-11-25
Rapid Plasma Genotyping For Early Initiation Of Erlotinib In EGFR Mutant Lung Cancer
CTID: NCT02770014
Phase: Phase 2    Status: Terminated
Date: 2019-11-22
TARCEVA (Erlotinib) in Combination With Chemoradiation in Patients With Stage IIIA/B Non-Small Cell Lung Cancer (NSCLC)
CTID: NCT00563784
Phase: Phase 2    Status: Completed
Date: 2019-11-20
A Phase I Study of MK-2206 in Combination With Standard Chemotherapy in Participants With Locally Advanced or Metastatic Solid Tumors (MK-2206-003)
CTID: NCT00848718
Phase: Phase 1    Status: Completed
Date: 2019-11-12
A Study of Emibetuzumab in Non Small Cell Lung Cancer (NSCLC) Participants
CTID: NCT01900652
Phase: Phase 2    Status: Completed
Date: 2019-09-18
Erlotinib in Combination With Temozolomide in Treating Relapsed/Recurrent/Refractory Pediatric Solid Tumors
CTID: NCT02689336
Phase: Phase 2    Status: Withdrawn
Date: 2019-09-09
Erlotinib or Placebo Following Chemoradiotherapy (Chemo/RT) in Stage III Non-Small Cell Lung Cancer (NSCLC)
CTID: NCT00153803
Phase: Phase 3    Status: Completed
Date: 2019-09-06
Molecularly Determined Treatment of Diffuse Intrinsic Pontine Gliomas (DIPG)
CTID: NCT01182350
Phase: Phase 2    Status: Terminated
Date: 2019-09-04
Erlotinib Hydrochloride With or Without Carboplatin and Paclitaxel in Treating Patients With Stage III-IV Non-small Cell Lung Cancer
CTID: NCT00126581
Phase: Phase 2    Status: Completed
Date: 2019-08-07
Erlotinib Hydrochloride or Crizotinib and Chemoradiation Therapy in Treating Patients With Stage III Non-small Cell Lung Cancer
CTID: NCT01822496
Phase: Phase 2    Status: Terminated
Date: 2019-08-05
An Extension Study of Onartuzumab in Participants With Solid Tumors on Study Treatment Previously Enrolled in a Company Sponsored Study
CTID: NCT02488330
Phase: Phase 3    Status: Completed
Date: 2019-07-23
Single-agent Erlotinib in Patients Previously Treated With Oral Etoposide in Protocol OSI-774-205
CTID: N e.querySelector("font strong").innerText = 'View More'

Biological Data
  • Erlotinib

  • Erlotinib
  • Erlotinib
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