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Posted by Dupont on 29.11.2016 11:29:06: erlotinib safe handling

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ТЕМА: Posted by Dupont on 29.11.2016 11:29:06: erlotinib safe handling

Posted by Dupont on 29.11.2016 11:29:06: erlotinib safe handling 7 года 5 мес. назад #914

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Tarceva 150 Mg 30 Comprimidos - Roche
– Carcinoma pancreatico (Tarceva somministrato in concomitanza con la gemcitabina nello studio PA.3) :
Hola me interesa el Tarceva, en cuanto lo esta vendiendo. A donde me puedo comunicar con usted. Me urge Saludos
forum.aide.ru/viewtopic.php?p=14507#14507
Grapefruit and grapefruit juice erlonat 150 mg price may interact with each viread peru medication. I will never take this medication for longer than recommended. This list is not known whether Ambien will harm an unborn baby.
erlotinib is used to treat non-small cell lung cancer (NSCLC), pancreatic cancer and several other types of cancer. It is a reversible tyrosine kinase inhibitor, which acts on the epidermal growth factor receptor (EGFR).
I've been on Tarceva just over 9 months. for NSCLC. Started with 3 tumors. One is gone, one is now scar tissue and one is reduced to 5mm. Used Elidel for rash and put up with other side effects. I just stopped for 2 months to give me body and chance to recoup. Next CT scan 6/11, if tuor is still 5mm I'll wait to go back, please pray for me. So far this has been a miracle.
Erlonat - Erlotinib belongs to a class of medications called kinase inhibitors. Erlotinib drug belongs to Epidermal Growth Factor Receptor (EGFR) tyrosine kinase inhibitors class of medicines. It is required in cancer chemotherapy medication and is mostly preferred for the treatment of non-small cell lung cancer. Consumption of this medicine interferes with the growth of cancer cells and helps in slowing down their growth in the human body. This drug is indicated for treatment of the patients suffering from advanced or metastatic non-small cell lung cancer.
If you have an allergy to erlotinib or any other part of this drug. Tell your doctor if you are allergic to any drugs. Make sure to tell about the allergy and what signs you had. This includes telling about rash; hives; itching; shortness of breath; wheezing; cough; swelling of face, lips, tongue, or throat; or any other signs. If you are pregnant or may be pregnant. If you are breast-feeding.
[Show abstract] [hide] ABSTRACT: Erlotinib is a tyrosine kinase inhibitor with anti epidermal growth factor receptor activity, approved as first line treatment concurrently administrated with gemcitabine for locally advanced unresectable or metastatic pancreatic cancer. One of the most common side effects, rash, is possibly linked to overall and progression-free survival and may serve as a potential surrogate marker. Nevertheless, erlotinib-induced rash is cause of negative impact on patients' quality of life and often can trigger discontinuation of treatment. Adequate and timely management of rash depending on the grade of rash is important for therapy continuation.
Complete information of erlonat tablets:
www.script-nn.ru/index.php/forum/раздел-...ancreatic-cancer#442
Tarceva studies and availability
Also reported herein is a process for the preparation of crystalline erlotinib hydrochloride Form R, which comprises:
17. The process according to claim 15. wherein said non-aqueous solvent system is trifluorotoluene and said anhydrous erlotinib hydrochloride is Form E.
Specific EGFR TKIs, such as gefitinib and erlotinib, gained FDA approval for the treatment of advanced NSCLC in 2003 and 2004, respectively. The clinical data gathered thus far indicates that only patients whose tumors harbor distinct activating mutations in the TK domain of the receptor are likely to benefit from first-line treatment with EGFR TKIs. These mutations, typically exon 19 in-frame deletions (approximately 45%) and the L858R point mutation in exon 21 (40% to 45%), are detected in 10% to 30% of NSCLC patients [ 38. 39 ]. The relatively limited prevalence of these sensitizing mutations requires that the EGFR mutational status be verified prior to the initiation of first-line therapy with EGFR TKIs. To date, targeted mutation testing uses specific and sensitive methods, yet it requires tumor biopsy. This approach is invasive and lengthy with regard to the time required for mutation analysis and provides information about the sampled site alone. Moreover, it is not favorable for obtaining molecular information in the long term, as would be required during EGFR TKI therapy, owing to the development of secondary mutations in the receptor and subsequent resistance to TKI treatment [ 1. 6 ].
Five hundred thirty patients had at least one measurable lesion and were assessable for response. The complete plus partial response rate was 8.6% with erlotinib and gemcitabine and 8.0% with placebo and gemcitabine, and the median duration of response was 163 days in both arms. The incidence of stable disease was 48.9% with erlotinib and gemcitabine and 41.2% with placebo and gemcitabine. The overall disease control rate (complete response plus partial response plus stable disease) was 57.5% on erlotinib and gemcitabine and 49.2% on placebo and gemcitabine ( P = .07).
alliance.pp.ua/index.php?option=com_kune...1&id=1073&Itemid=145
Regulatory submissions are based on positive data from LUX-Lung 8 study that showed a significant delay in progression of lung cancer (progression-free survival, primary endpoint) and a significant improvement in overall survival for Giotrif (afatinib) compared to Tarceva (erlotinib)
www.blago-svet.com.ua/index.php?option=c...id=5740&lang=en#5740
A Phase II Single Arm Clinical Trial to Evaluate the Efficacy and Safety of the Combination of Tarceva™ (Erlotinib Hydrochloride) and Rapamune™ (Sirolimus) in the Treatment of Metastatic Renal Cell Carcinoma.
Erlotinib and gefitinib (n = 6)
Wacker B. Nagrani T. Weinberg J. Witt K. Clark G. Cagnoni PJ. Correlation between development of rash and efficacy in patients treated with the epidermal growth factor receptor tyrosine kinase inhibitor erlotinib in two large phase III studies. Clin Cancer Res 2007;13:3913-3921 CrossRef | Web of Science | Medline
Lu J, Eppler SM, Lum BL, Hamilton M, Rakhit A, Gaudreault J. A population pharmacokinetic (PK) model for erlotinib (E), a small molecule inhibitor of the epidermal growth factor receptor (EGFR) [abstract 2032]. J Clin Oncol 2005 ; 23. 143s.
Erlotinib Impurity 13
Maximum change from baseline in the sum of the longest diameters of target lesions (as assessed by the investigator per RECIST) . "Unevaluable" refers to patients who had a response assessment before the scheduled first assessment without an additional postbaseline assessment. 1 = 50 mg QD + gemcitabine/erlotinib; 2 = 75 mg BID + gemcitabine/erlotinib; 3 = 125 mg QD + gemcitabine/erlotinib; 4 = 100 mg QD + gemcitabine/erlotinib; 5 = 100 mg QD + erlotinib; 6 = 125 mg QD + erlotinib.
Function: Other Brand Name: Erlotinib Strength: 25 mg Dosage Form: Tablets
www.autogrodno.by/kunena/30/22006-posted...otinib-3rd-line.html
19. Lainey E, Wolfromm A, Marie N, Enot D, Scoazec M, Bouteloup C, et al. Azacytidine and erlotinib exert synergistic effects against acute myeloid leukemia. Oncogene. 2012 In press. [PubMed ]
Experimental: Arm B (erlotinib hydrochloride, bevacizumab)
Additional preclinical and clinical investigations are ongoing to identify whether alternative schedules and or dosing regimens might allow erlotinib to be combined with chemotherapy in patients with first-line stage IIIB/IV disease. In addition, the identity of clinical or molecular surrogates that may predict for improved outcome (ie, never smokers or somatic mutation in the kinase domain of EGFR) are still preliminary and will require further investigation in prospective, randomized trial settings.
Before taking Tarceva, tell your doctor if you have lung problems (other than lung cancer), kidney or liver disease, if you are dehydrated, or if you smoke.
Lecaer H, Barlesi F, Corre R, Jullian H, Bota S, Falchero L, Vergnenegre A, Dujon C, Delhoume JY, Chouaid C: A multicentre phase II randomised trial of weekly docetaxel/gemcitabine followed by erlotinib on progression, vs the reverse sequence, in elderly patients with advanced non small-cell lung cancer selected with a comprehensive geriatric assessment (the GFPC 0504 study). Br J Cancer. 2011, 105: 1123-1130. 10.1038/bjc.2011.331. CrossRef PubMed PubMedCentral Google Scholar
iamwithyouforever.org/index.php/ru/forum...-mechanism-of-action
Any prior treatment with erlotinib or other agent whose primary mechanism of action is known to inhibit EGFR
DOTAP:Chol-fus1, Erlotinib, Dexamethasone, Diphenhydramine
Eltrombopag, Erlotinib, Ticagrelor, Ramucirumab, Romiplostin: EMA empfiehlt Erweiterung der Zulassung
test1.saitrus.ru/kunena/razdel-predlozhe...otinib-tarceva-forum
Erlotinib is a potent inhibitor of CYP1A1 and UGT1A1 and a moderate inhibitor of CYP3A4 and CYP2C8. However, the relevance of these in vitro data to clinical practice has not been elucidated.
To study GLE's effect in IBC cells with acquired Erlotinib resistance, we successfully developed stable Erlotinib resistant cells (rSUM-149). Higher Erlotinib concentrations did not affect viability of resistant cells while GLE reduced rSUM-149 cell viability in a concentration dependent manner (Fig. 3 A). However, Erl/GLE significantly decreased cell viability compared to Erlotinib but not against GLE as observed on Erlotinib sensitive SUM-149 cells. To determine the effectiveness of Erl/GLE in rSUM-149 cells, we calculated the CIs at a CR ratio (1:24;Erl:GLE), and at a NCR combining Erl+0.2 mg/mL-GLE. The Fa-CI plot (Fig. 3

and Table 3 show that the rSUM-149 ED 50 CI value was similar to that in parental cells (0.76 vs 0.61). However, the CIs increased as the effective dose increased, transforming the synergic effect into antagonistic. As expected, Dm for Erl/GLE was less (0.26) than Erlotinib (31.7) and GLE (0.33). Furthermore, only Erl/GLE disrupted rSUM-149 cell spheroid formation (Fig. 3 C). Next, we studied the effect of Erl/GLE in intrinsically Erlotinib resistant BC cells by treating MDA-MB-231 cells under the same conditions as rSUM149. GLE reduced cell viability in a concentration dependent manner (Fig. 3 D), while Erl/GLE significantly decreased cell viability compared to Erlotinib or GLE. In a CR, Erl/GLE, MDA-MB-231 ED 50 CI value was 0.22 (synergism). The sensitivity level of these cells to GLE was 0.35 mg/mL, similar to rSUM-149 cells (0.33mg/mL). At a NCR, most of the concentrations tested with GLE were antagonists. However, two of them were synergic and one showed an additive effect (Fig. 3 E and Table 3 ). These results suggest that an Erl/GLE synergic effect is observed in EGFR-overexpressing BC cells with acquired and intrinsic resistance.
A series of SEDDS formulations were prepared and their self-emulsifying properties were visually observed. A pseudo-ternary phase diagram was constructed in the absence of erlotinib for identification of the self-emulsifying regions and to optimize the concentration of oil, surfactant, and co-surfactant in the liquid SEDDS formulation ( 32. 35 ). The phase diagram of the system containing Labrasol as the surfactant, Labrafil M2125CS as the oil, and Transcutol HP as the co-surfactant is shown in Fig. 1. As can be seen, the self-emulsifying region which is described by the black color accounts for 10% of the total area. Spontaneous emulsion formation was not efficient when the amount of surfactant was less than 50% in the liquid SEDDS. The efficiency of emulsification was good when the total concentration of the surfactant/co-surfactant was more than 75% w / w of the liquid SEDDS formulation. The formulations surrounding the self-emulsifying domain exhibited poor emulsion forming ability. It has been reported that incorporation of the drug into the liquid SEDDS may have some effects on self-emulsifying performance of the system. In our study, significant differences were found in self-emulsifying performance when compared with the corresponding formulations with 6% ( w / w ) of erlotinib. The reason may be to increase the solvent capacity of the formulations for the drug with intermediate log P value (2 < log P < 4), high content of hydrophilic surfactant and co-surfactant was used. When the formulations were dispersed into aqueous solutions, the hydrophilic substances had the tendency to separate from the oil to be dissolved in water phase, causing phase separation and partial drug precipitation ( 39 ).
Background: G and E have shown a survival benefit in the 1 st -line setting in mPC. The aim of this study was to assess whether combining C with G+E was safe and effective as compared with G-E in patients(pts) with mPC. Methods: Previously untreated pts with mPC were randomized in a 1:1 ratio to receive G(1000 mg/m2, d1,8,15)+E(100 mg, d1–28)+C(1660 mg/m2, d1-21) or G+E, q4-wk, until progression or unacceptable toxicity. Primary endpoint: progression-free survival (PFS); secondary endpoints: overall survival (OS), response rate (RR), relationship of rash with PFS/OS, and safety. A sample size of 118 pts was required for a hazard ratio(HR) of 0.63, assuming a median PFS of 6 months (m) in pts treated with GEC; unilateral α=0.05; β=0.8. Results: 120 pts were randomized. Median age: 63 years; ECOG status 0/1/2(%), 33/58/8. Median follow-up was 16.5 m (95%CI:13.7-26.2). Median PFS was 4.3 m in the GEC arm and 3.8m in the GE arm (HR:0.88; 95%CI:0.58-1.31; p=0.52). The estimated median OS was 6.8 m in the GEC arm as compared with 7.7 m in the GE group (HR:1.09, 95%CI:0.72-1.63; p=0.69). Neutropenia grade 3/4 (GEC 43% vs GE 15%; p=0.0008) and mucositis (GEC 9% vs GE 0%;p=0.03), were the only statistically significant differences in grade 3/4 adverse events. PFS and OS were significantly longer in pts with rash (grade ≥ 1) vs no rash (grade=0): PFS 5.5 vs 2.0 m; HR=0.39 95%CI:0.26-0.6; p<0.0001 and OS: 9.5 vs 4.0 m; HR=0.51 95%CI:0.33-0.77; p=0.0014). Conclusions: PFS with GEC was not different to that with GE as it did not meet the criterion for statistical significance. Skin rash strongly predicted erlotinib efficacy, deserving further investigation for patient selection. Clinical trial information: NCT01303029.
China Leverancier Erlotinib hcl, gratis Monsters Erlotinib Hydrochloride CAS 183319-69-9
In recent years, a number of TKIs (tyrosine kinase inhibitors) targeting epidermal growth factor receptor (EGFR) family have been synthesized and some have been approved for clinical treatment of cancer by the FDA. We recently reported a new pharmacological action of the 4-anilinoquinazoline derived EGFR TKIs, such as lapatinib (Tykerb®) and erlotinib (Tarceva®), which significantly affect the drug resistance patterns in cells expressing the multidrug resistance (MDR) phenotype. Previously, we showed that lapatinib and erlotinib could inhibit the drug efflux function of P-glycoprotein (P-gp, ABCB1) and ABCG2 transporters. In this study, we determined if these TKIs have the potential to reverse MDR due to the presence of the multidrug resistance protein 7 (MRP7, ABCC10). Our results showed that lapatinib and erlotinib dose-dependently enhanced the sensitivity of MRP7-transfected HEK293 cells to several established MRP7 substrates, specifically docetaxel, paclitaxel, vinblastine and vinorelbine, whereas there was no or a lesser effect on the control vector transfected HEK293 cells. [ 3 H]-paclitaxel accumulation and efflux studies demonstrated that lapatinib and erlotinib increased the intracellular accumulation of [ 3 H]-paclitaxel and inhibited the efflux of [ 3 H]-paclitaxel from MRP7 transfected cells but not in the control cell line. Lapatinib is a more potent inhibitor of MRP7 than erlotinib. In addition, the Western blot analysis revealed that both lapatinib and erlotinib did not significantly affect MRP7 expression. We conclude that the EGFR TKIs, lapatinib and erlotinib reverse MRP7-mediated MDR through inhibition of the drug efflux function, suggesting that an EGFR TKI based combinational therapy may be applicable for chemotherapeutic practice clinically.
I. Determine the relationship between erlotinib dose-schedule and immuno-histochemical staining pattern of phospho-ERK, PCNA, EGF, and alpha smooth muscle actin (alphaSMA) in the liver.