1 film-coated tablet contains 27.32 mg of erlotinib hydrochloride, equivalent to 25 mg of erlotinib or 109.27 mg of erlotinib hydrochloride, equivalent to 100 mg of erlotinib, or 163.90 mg of erlotinib hydrochloride, equivalent to 150 mg of erlotinib;
film coating: polyvinyl alcohol, titanium dioxide (E 171), macrogol, talc, methacrylate copolymer (type A), sodium bicarbonate.
Dosage form
Film-coated tablets.
Main physicochemical properties:
25 mg tablets: round, biconvex, film-coated tablets, white to yellowish in color, engraved with "25" on one side;
100 mg tablets: round, biconvex, film-coated tablets, white to yellowish in color, engraved with "100" on one side;
150 mg tablets: round, biconvex, film-coated tablets, white to yellowish in color, engraved with "150" on one side.
Pharmacotherapeutic group
Antineoplastic agents. Protein kinase inhibitors. Erlotinib. ATC code L01E B02.
Pharmacological properties
Pharmacodynamics.
Erlotinib is a tyrosine kinase inhibitor of the epidermal growth factor receptor/human epidermal growth factor receptor type 1 (EGFR, also known as HER1). Erlotinib causes a marked inhibition of intracellular phosphorylation of EGFR. EGFR is expressed on the cell surface of both normal and cancer cells. In preclinical models, inhibition of EGFR phosphotyrosine leads to cell growth arrest/death. EGFR-activating mutations can lead to persistent activation of anti-apoptotic and proliferative signaling pathways. The high efficacy of erlotinib in blocking EGFR-mediated signaling in such EGFR mutation-positive tumors is explained by the tight binding of erlotinib to the ATP-binding site in the mutated EGFR kinase domain. By blocking downstream signaling, cell proliferation is arrested and cell death is induced by natural apoptosis. In mouse models of overexpression of these EGFR-activating mutations, tumor regression is observed.
Pharmacokinetics.
Absorption.
Peak plasma concentrations of erlotinib are reached approximately 4 hours after oral administration. A study in healthy volunteers estimated the absolute bioavailability of the drug to be 59%. Oral exposure may be increased by food.
Distribution.
Erlotinib has a mean apparent volume of distribution of 232 L and is distributed into human tumor tissues. In a study of 4 patients (3 with non-small cell lung cancer [NSCLC] and 1 with laryngeal cancer) receiving Erlotinib 150 mg daily, tumor samples obtained at surgery on day 9 contained a mean erlotinib concentration of 1185 ng/g tissue. This corresponds to an overall mean of 63% (range 5 to 161%) of the steady-state maximum plasma concentration. The primary active metabolites were present in the tumor at a mean concentration of 160 ng/g tissue, corresponding to an overall mean of 113% (range 88 to 130%) of the steady-state maximum plasma concentration. Plasma protein binding is approximately 95%. Erlotinib binds to serum albumin and alpha-1-acid glycoprotein (AAG).
Metabolism.
Erlotinib is metabolized in the liver by hepatic cytochromes of the cytochrome system, mainly involving CYP3A4 and, to a lesser extent, CYP1A2. Extrahepatic metabolism of erlotinib occurs via CYP3A4 in the small intestine, CYP1A1 in the lungs, and CYP1B1 in tumor tissue, which may also be involved in the metabolic clearance of erlotinib. Metabolism occurs via three pathways: 1) O-dimethylation of one or both side chains followed by oxidation to carboxylic acids; 2) oxidation of the acetylenic moiety followed by hydrolysis to arylcarboxylic acids; 3) aromatic hydroxylation of the phenyl-acetylenic group. The primary metabolites of erlotinib, OSI-420 and OSI-413, which are formed by O-demethylation of one of the side chains, are comparable in potency to erlotinib in preclinical in vitro assays and in vivo tumor models. They are present in plasma at concentrations <10% of those of erlotinib and have pharmacokinetics similar to those of erlotinib. Elimination
Erlotinib metabolites are excreted primarily in the feces (>90%), with a small amount of the oral dose excreted renally (approximately 9%). Less than 2% of the oral dose is excreted as parent compound. A population pharmacokinetic analysis of 591 patients treated with Erlotinib as monotherapy showed a mean apparent clearance of 4.47 L/h with a median elimination half-life of 36.2 hours. Therefore, the time to reach steady-state plasma concentrations is expected to be approximately 7–8 days.
Population pharmacokinetic analysis revealed no clinically relevant relationships between predicted apparent clearance and patient age, weight, gender or ethnicity. Erlotinib pharmacokinetics were dependent on serum total bilirubin, alpha-1-acid glycoprotein (AAG) and current smoking status. Erlotinib clearance was decreased with increasing total bilirubin and alpha-1-acid glycoprotein concentrations. The clinical significance of this finding is unknown. However, smokers have been shown to have an increased clearance of erlotinib, which was confirmed in a pharmacokinetic study of a single dose of 150 mg erlotinib in non-smokers and current smokers. The geometric mean peak concentration was 1056 ng/mL in non-smokers and 689 ng/mL in smokers, with a mean ratio of 65.2% (95% CI: 44.3-95.9; p = 0.031). The geometric mean AUC0-inf was 18726 ng h/mL in non-smokers and 6718 ng h/mL in smokers, with a mean ratio of 35.9% (95% CI: 23.7-54.3; p < 0.0001). The geometric mean concentration at 24 hours was 288 ng/mL in nonsmokers and 34.8 ng/mL in smokers with a mean ratio of 12.1% (95% CI: 4.82–30.2; p = 0.0001).
In a pivotal phase III study, in patients with non-small cell lung cancer who were smokers, the trough steady-state plasma concentration was 0.65 μg/mL (n=16), which was 2-fold lower than in patients with previous smoking/non-smokers (1.28 μg/mL, n=108). This was accompanied by a 24% increase in erlotinib plasma clearance. In a phase I dose-escalation study in patients with NSCLC who were smokers during the study, steady-state pharmacokinetic analysis showed a dose-proportional increase in erlotinib exposure following an increase in the dose of Erlotinib-Vista from 150 mg to the maximum tolerated dose of 300 mg. The steady-state trough plasma concentration after a 300 mg dose in continuing smokers in this study was 1.22 μg/ml (n=17) (see sections 4.2, 4.4, and 4.5).
Based on the results of pharmacokinetic studies, smokers are advised to stop smoking while taking Erlotinib-Vista, as otherwise plasma concentrations of the drug may be reduced.
Based on population pharmacokinetic analysis, erlotinib exposure increased by approximately 11% in the presence of opioids.
A second population pharmacokinetic analysis was performed using erlotinib data from 204 patients with pancreatic cancer receiving erlotinib in combination with gemcitabine. This analysis showed that the covariates that affected erlotinib clearance in patients with pancreatic cancer were essentially the same as in previous pharmacokinetic analyses in monotherapy. No new covariate effects were identified. Concomitant gemcitabine administration did not affect erlotinib plasma clearance.
Children.
No specific studies involving children have been conducted.
Elderly patients.
No specific studies have been conducted in elderly patients.
Liver dysfunction.
Erlotinib is cleared primarily by the liver. In patients with solid tumors and moderate hepatic impairment (Child-Pugh score 7-9), the geometric mean AUC0-t and Cmax of erlotinib were 27,000 ng h/mL and 805 ng/mL, respectively, compared with 29,300 ng h/mL and 1,090 ng/mL in patients with normal hepatic function, including patients with primary liver cancer or liver metastases. Although Cmax was statistically significantly lower in patients with moderate hepatic impairment, this difference is not considered clinically significant. There is no evidence of the effect of severe hepatic dysfunction on the pharmacokinetics of erlotinib. In a population pharmacokinetic analysis, increased serum total bilirubin concentrations were associated with a slower rate of erlotinib elimination.
Kidney dysfunction.
Erlotinib and its metabolites are excreted by the kidneys in insignificant amounts - less than 9% of a single dose is excreted in the urine. In a population pharmacokinetic analysis, no clinically significant relationship was observed between erlotinib clearance and creatinine clearance. There are no data in patients with creatinine clearance <15 ml/min.
Indication
Non-small cell lung cancer.
First-line treatment of patients with locally advanced or metastatic non-small cell lung cancer with EGFR-activating mutations.
Erlotinib-Vista is also indicated for the transition to maintenance treatment of patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with EGFR-activating mutations and stable disease after first-line chemotherapy.
Factors associated with prolonged survival should be considered when prescribing Erlotinib-Vista. No survival benefit or other clinically meaningful treatment effects have been demonstrated in patients with tumors that lack epidermal growth factor receptor (EGFR) immunohistochemistry.
Pancreatic cancer.
Treatment of metastatic pancreatic cancer, in combination with gemcitabine. When prescribing Erlotinib-Vista, factors associated with prolonged survival should be considered.
No survival benefit has been demonstrated in patients with locally advanced pancreatic cancer.
Contraindication
Hypersensitivity to erlotinib or to any component of the drug.
Interaction with other medicinal products and other types of interactions
Interaction studies have only been conducted in adult patients.
Erlotinib and other CYP substrates.
Erlotinib is a potent inhibitor of CYP1A1 and a moderately potent inhibitor of CYP3A4 and CYP2C8, as well as a potent inhibitor of UGT1A1 glucuronidation in vitro.
The physiological significance of potent CYP1A1 inhibition is unknown due to the very limited expression of CYP1A1 in human tissues.
When erlotinib was administered with ciprofloxacin, a moderately potent CYP1A2 inhibitor, erlotinib exposure (AUC) increased by 39%, while the maximum concentration (Cmax) was not statistically significantly changed. Similarly, the exposure (AUC) of the active metabolites increased by 60% and 48% for AUC and Cmax, respectively. The clinical significance of this increase in exposure has not been established. Therefore, caution should be exercised when prescribing Erlotinib-Vista with ciprofloxacin or potent CYP1A2 inhibitors (e.g. fluvoxamine). If adverse reactions related to erlotinib are observed, the dose of the drug can be reduced.
Pretreatment or concomitant use of Erlotinib-Vista did not alter the clearance of the prototypical CYP3A4 substrates midazolam and erythromycin. However, a decrease in oral bioavailability of midazolam of up to 24% was observed. In another clinical study, erlotinib was shown not to affect the pharmacokinetics of the CYP3A4/2C8 substrate paclitaxel when co-administered. Therefore, significant interactions with the clearance of other CYP3A4 substrates are unlikely. Inhibition of glucuronidation may result in interactions with drugs that are substrates of UGT1A1 and are eliminated exclusively by this metabolic pathway. Patients with low levels of UGT1A1 expression or genetically determined disorders of glucuronidation (e.g. Gilbert syndrome) may experience increased serum bilirubin concentrations and should be treated with caution.
Erlotinib is metabolized in the liver by hepatic cytochromes, primarily CYP3A4 and, to a lesser extent, CYP1A2. Extrahepatic metabolism by CYP3A4 in the small intestine, CYP1A1 in the lung, and CYP1B1 in tumor tissue also potentially contribute to the metabolic clearance of erlotinib. Potential interactions with active substances that are metabolized by, or are inducers or inhibitors of, these enzymes are possible.
Potent CYP3A4 inhibitors reduce the metabolism of erlotinib and increase its plasma concentrations. In a clinical study, co-administration of erlotinib with ketoconazole (200 mg orally twice daily for 5 days), a potent CYP3A4 inhibitor, resulted in an increase in erlotinib exposure (86% AUC and 69% Cmax). Caution should be exercised when prescribing Erlotinib-Vista with potent CYP3A4 inhibitors, in particular azole antifungals (ketoconazole, itraconazole, voriconazole), protease inhibitors, erythromycin, clarithromycin. In case of toxicity, the dose of Erlotinib-Vista should be reduced.
Strong CYP3A4 inducers increase the metabolism of erlotinib and significantly decrease its plasma concentrations. In a clinical study, co-administration of erlotinib with rifampicin (600 mg orally once daily for 7 days), a strong CYP3A4 inducer, resulted in a 69% decrease in median erlotinib AUC. When rifampicin was co-administered with a single 450 mg dose of Erlotinib, the mean erlotinib exposure (AUC) was 57.5% of that after a single 150 mg dose of Erlotinib in the absence of rifampicin therapy. Co-administration of Erlotinib and CYP3A4 inducers should be avoided. For patients requiring concomitant treatment with Erlotinib and a strong CYP3A4 inducer (such as rifampicin), an increase in the Erlotinib dose to 300 mg should be considered with close monitoring of the patient's condition (including renal function, liver function, and serum electrolytes). If well tolerated for more than 2 weeks, the Erlotinib dose may be increased to 450 mg with close safety monitoring. Reduced exposure to erlotinib may occur with concomitant use of other CYP3A4 inducers (phenytoin, carbamazepine, barbiturates, St. John's wort). These agents should be used with caution in combination with erlotinib. Alternative agents that are not strong CYP3A4 inducers should be considered whenever possible.
Elevations in international normalized ratio (INR) and bleeding, including some fatal cases, have been reported with the use of erlotinib and coumarin anticoagulants, including warfarin. Patients receiving coumarin anticoagulants should have their prothrombin time or INR monitored regularly.
Erlotinib and statins.
The risk of statin-induced myopathy, including rhabdomyolysis, which has been observed rarely, may be increased when Erlotinib is used in combination with statins. Erlotinib and patients who smoke.
The results of a pharmacokinetic study in non-smokers and current smokers showed that smoking reduces the AUCinf, Cmax and plasma concentration of erlotinib after 24 hours by 2.8, 1.5 and 9 times, respectively. Therefore, smokers should be advised to stop smoking as early as possible before starting treatment with Erlotinib-Vista due to the decrease in plasma concentrations of erlotinib with continued smoking. Based on the results of the CURRENTS study, there was no evidence to support the use of the higher dose of 300 mg of erlotinib in active smokers compared to the recommended dose of 150 mg. The safety profile was comparable for the 300 mg and 150 mg doses; however, a significant increase in the incidence of rash, interstitial lung disease and diarrhoea was observed in patients receiving higher doses of erlotinib (see sections 4.2, 4.4, and 5.2).
Erlotinib and P-glycoprotein inhibitors.
Erlotinib is a substrate for the P-glycoprotein drug transporter. Concomitant use of Erlotinib and P-glycoprotein inhibitors (e.g. cyclosporine and verapamil) may result in impaired distribution and/or elimination of erlotinib. The consequences of this interaction, particularly for the central nervous system, such as toxicity, have not been established. Caution should be exercised in such situations.
Erlotinib and drugs that affect pH.
Erlotinib has reduced solubility at pH levels above 5. Drugs that affect upper gastrointestinal pH may affect erlotinib solubility and bioavailability. When erlotinib was co-administered with omeprazole, a proton pump inhibitor, erlotinib exposure (AUC) and Cmax were decreased by 46% and 61%, respectively. There was no change in Tmax or half-life. When erlotinib was co-administered with ranitidine (300 mg), an H2-receptor antagonist, erlotinib exposure (AUC) and Cmax were decreased by 33% and 54%, respectively. It is unlikely that an increase in the dose of erlotinib when co-administered with such drugs would compensate for the decrease in exposure. However, when erlotinib was administered 2 hours before or 10 hours after ranitidine (150 mg twice daily), erlotinib AUC and Cmax were reduced by only 15% and 17%, respectively. The effect of antacids on the absorption of erlotinib has not been studied, but it is possible that the absorption of erlotinib may be impaired, which could lead to a decrease in erlotinib plasma levels. Therefore, combinations of erlotinib with proton pump inhibitors should be avoided. If antacid therapy is necessary during the use of Erlotinib-Vista, these drugs should be taken at least 4 hours before or 2 hours after the daily dose of Erlotinib-Vista. If ranitidine is prescribed, its administration should be alternated with Erlotinib-Vista: the drug should be taken at least 2 hours before or 10 hours after taking ranitidine.
Erlotinib and gemcitabine.
In the phase Ib study, no significant effect of gemcitabine on the pharmacokinetics of erlotinib, nor of erlotinib on the pharmacokinetics of gemcitabine, was observed.
Erlotinib and carboplatin/paclitaxel.
Erlotinib increases plasma platinum concentrations. In a clinical study, co-administration of erlotinib with carboplatin and paclitaxel resulted in a statistically significant increase in total platinum AUC0-48 exposure of 10.6%, but this is not clinically relevant. In clinical practice, other concomitant factors may be involved, such as renal impairment, that increase carboplatin exposure. No significant effect of carboplatin or paclitaxel on the pharmacokinetics of erlotinib was observed.
Erlotinib and capecitabine.
Capecitabine may increase erlotinib concentrations. Erlotinib in combination with capecitabine resulted in a statistically significant increase in erlotinib AUC and a marginal increase in Cmax compared to values obtained in another study in which erlotinib was administered as monotherapy. Erlotinib did not have a significant effect on the pharmacokinetics of capecitabine.
Erlotinib and proteasome inhibitors.
Based on their mechanism of action, proteasome inhibitors, including bortezomib, would be expected to interfere with the action of epidermal growth factor receptor (EGFR) inhibitors, including erlotinib. Limited clinical data and preclinical studies demonstrating proteasome-mediated degradation of EGFR support this.
Application features
When deciding whether to use Erlotinib-Vista as first-line or maintenance treatment for locally advanced or metastatic NSCLC, it is important to determine EGFR mutation status.
A validated, reliable and sensitive test with a defined positivity cut-off and demonstrated utility in determining EGFR mutation status using tumor DNA from a tissue sample or free circulating DNA (fcc) from a blood (plasma) sample should be used, in accordance with local medical practice.
If a plasma-based tsDNA test is used and the activating mutation results are negative, a tissue test should be performed if possible, as there is a possibility of false negative results with the plasma-based test.
Use in patients who smoke.
Smokers should be advised to stop smoking, as erlotinib plasma concentrations are reduced in smokers compared to non-smokers. The extent of the reduction in erlotinib plasma concentrations is likely to be clinically relevant (see sections 4.2, 4.5, and 5.2).
Interstitial lung disease.
Interstitial lung disease (ILD)-like events, including fatal ILD, have been reported uncommonly in patients with non-small cell lung cancer, pancreatic cancer, or other advanced solid tumors treated with erlotinib. In the pivotal BR.21 study in patients with non-small cell lung cancer treated with placebo or erlotinib, the incidence of ILD was 0.8% in each group. In a meta-analysis of randomized controlled clinical trials of NSCLC (excluding single-arm phase I and phase II studies due to the lack of control groups), the incidence of ILD-like events was 0.9% in the erlotinib groups and 0.4% in the control groups. In a pancreatic cancer study in combination with gemcitabine, the incidence of ILD-like events in pancreatic cancer patients treated with erlotinib and gemcitabine was 2.5% compared to 0.4% in the gemcitabine and placebo group. Reported diagnoses in patients with suspected ILD-like events included pneumonitis, radiation pneumonitis, hypersensitivity pneumonitis, interstitial pneumonia, interstitial lung disease, bronchiolitis obliterans, pulmonary fibrosis, acute respiratory distress syndrome (ARDS), lung infiltration, and alveolitis. Symptoms occurred within days to months of starting erlotinib therapy. Confounding or predisposing factors such as concomitant or prior chemotherapy, radiotherapy, underlying parenchymal lung disease, metastatic lung disease or pulmonary infection were often present. A higher incidence of ILD (approximately 5% with a mortality rate of 1.5%) was observed in patients in studies conducted in Japan. In patients with acute onset of new and/or progressive pulmonary symptoms of unexplained origin (dyspnea, cough and fever), erlotinib should be temporarily discontinued pending diagnostic evaluation. Patients receiving concomitant treatment with erlotinib and gemcitabine should be closely monitored for the possible development of ILD-like toxicity. In the event of ILD, erlotinib should be discontinued and appropriate treatment initiated if necessary (see section 4.8).
Diarrhea, dehydration, electrolyte imbalance, and kidney failure.
Diarrhea (including very rare cases with a fatal outcome) has been observed in approximately 50% of patients treated with erlotinib. In the event of severe or moderate diarrhea, it is necessary to prescribe, for example, loperamide. In some cases, the dose of the drug should be reduced. In clinical studies, the dose was reduced in 50 mg increments. Dose reduction in 25 mg increments has not been studied. In case of severe or persistent diarrhea, nausea, anorexia or vomiting, accompanied by dehydration, Erlotinib should be discontinued and appropriate measures should be taken to eliminate dehydration (see section "Adverse reactions"). Cases of hypokalemia and renal failure (including fatal outcomes) have been reported rarely. In some cases, dehydration was due to diarrhea, vomiting, and/or anorexia, while in other cases, interpretation was complicated by concomitant chemotherapy. In more severe or persistent cases of diarrhea or cases leading to dehydration, especially in patient groups with aggravating risk factors (concurrent use of other drugs, presence of symptoms or diseases, or other predisposing factors, including older age), Erlotinib treatment should be interrupted and appropriate measures should be taken to intensively rehydrate the patient intravenously. In patients at risk of dehydration, renal function and serum electrolytes, including potassium, should also be monitored.
Cases of hepatic failure (including fatal outcomes) have been reported rarely with erlotinib. Confounding factors include pre-existing liver disease and concomitant use of hepatotoxic medicinal products. Therefore, periodic monitoring of liver function is recommended in this patient population. If significant changes in liver function occur, treatment with Erlotinib should be discontinued (see section 4.8). Erlotinib is not recommended for patients with severe hepatic impairment.
Gastrointestinal perforations.
Patients taking Erlotinib are at increased risk of gastrointestinal perforation, which has been reported infrequently (including some fatal cases). An increased risk of gastrointestinal perforation is seen in patients receiving concomitant treatment with antiangiogenic agents, corticosteroids, nonsteroidal anti-inflammatory drugs (NSAIDs) and/or taxane-based chemotherapy, and in patients with a history of peptic ulcer or diverticular disease. If gastrointestinal perforation occurs, Erlotinib should be permanently discontinued (see section 4.8).
Bullous and exfoliative skin lesions.
Bullous, bullous and exfoliative skin reactions, including very rare cases of Stevens-Johnson syndrome/toxic epidermal necrolysis, some of which were fatal, have been reported with erlotinib (see section 4.8). If bullous, bullous or exfoliative skin reactions occur, erlotinib should be temporarily withheld or discontinued. Patients with bullous or exfoliative skin reactions should be evaluated for skin infections and treated according to local treatment guidelines.
Visual impairment.
Patients who experience signs and symptoms consistent with keratitis, such as acute onset or worsening of the following: eye inflammation, tearing, photosensitivity, blurred vision, pain and/or redness, should be referred immediately to an ophthalmologist. If a diagnosis of ulcerative keratitis is confirmed, erlotinib treatment should be temporarily or permanently discontinued. If a diagnosis of keratitis is made, the benefits and risks of continuing treatment with Erlotinib should be carefully weighed. Erlotinib should be used with caution in patients with a history of keratitis, ulcerative keratitis or severe dry eye. Wearing contact lenses is also a risk factor for keratitis and ulceration. Cases of corneal perforation or ulceration have been observed very rarely with erlotinib (see section 4.8).
Interaction with other drugs.
Strong inducers of CYP3A4 enzymes may reduce the efficacy of erlotinib, while strong inhibitors of CYP3A4 may lead to increased toxicity. Concomitant use of Erlotinib with these types of drugs should be avoided (see section 4.5).
Other forms of interaction.
Erlotinib has reduced solubility at pH levels above 5. Drugs that alter the pH of the upper gastrointestinal tract (GI) such as proton pump inhibitors, H2-receptor antagonists, antacids may affect the solubility of erlotinib and, consequently, its bioavailability. It is unlikely that an increase in the dose of Erlotinib-Vista when co-administered with these drugs would compensate for the decrease in its exposure. The concomitant administration of Erlotinib-Vista and proton pump inhibitors should be avoided. The effects of concomitant administration of erlotinib with H2-receptor antagonists and antacids are unknown, but bioavailability may be reduced. Therefore, concomitant administration should be avoided (see section 4.5). If antacid therapy is necessary during the use of Erlotinib-Vista, these drugs should be taken at least 4 hours before or 2 hours after taking the daily dose of Erlotinib-Vista.
Important information about excipients.
The medicine contains lactose and should not be used in patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption.
Each 25 mg film-coated tablet contains 23.98 mg of lactose monohydrate.
Each 100 mg film-coated tablet contains 95.93 mg of lactose monohydrate.
Each 150 mg film-coated tablet contains 143.90 mg of lactose monohydrate.
If the patient has been diagnosed with an intolerance to some sugars, contact your doctor before taking this medicinal product.
1 tablet of 25 mg of the drug Erlotinib-Vista contains 4.2036 mg of sodium.
1 tablet of 75 mg of the drug Erlotinib-Vista contains 16.8144 mg of sodium.
This medicine contains less than 1 mmol (less than 23 mg) sodium per tablet, i.e. essentially 'sodium-free'.
1 tablet of 100 mg of the drug Erlotinib-Vista contains 25.20216 mg of sodium.
Caution should be exercised when used in patients on a controlled sodium diet.
Disposal of unused and/or expired medicinal products. Release of medicinal products into the environment should be minimised. Medicinal products should not be disposed of in wastewater or household waste. For disposal, use a so-called “waste collection system” if available.
Use during pregnancy or breastfeeding.
Pregnancy.
There are no adequate data from the use of erlotinib in pregnant women. Animal studies have shown no evidence of teratogenic effects or birth defects. However, the possibility of adverse effects on pregnancy cannot be excluded, as an increased rate of embryo-fetal lethality was observed in animal studies. The potential risk to humans is unknown. Women of childbearing potential are advised to avoid pregnancy and to use reliable methods of contraception during treatment with Erlotinib-Vista for at least 2 weeks after completion of treatment. Treatment of a pregnant woman should be continued only if the expected benefit to the mother outweighs the potential risk to the fetus.
Breast-feeding.
It is not known whether erlotinib is excreted in human milk.
Studies on the effects of erlotinib on milk production or its presence in human milk have not been conducted. Because the potential harm to breastfed infants is unknown, it is recommended that nursing mothers discontinue breastfeeding while taking the drug and for at least 2 weeks after the last dose.
Fertility.
Animal studies indicate no impairment of fertility. However, the possibility of an adverse effect on fertility cannot be excluded, as effects on reproductive performance have been shown in animal studies. The potential risk for humans is unknown.
The ability to influence the reaction speed when driving vehicles or other mechanisms.
Studies on the effect on the ability to drive or operate machinery have not been conducted, but the effect of erlotinib does not involve impairment of mental activity.
Method of administration and doses
Treatment with Erlotinib-Vista should be carried out by a doctor who has experience in the use of anticancer therapy.
Non-small cell lung cancer.
Before initiating treatment with Erlotinib, patients with advanced or metastatic non-small cell lung cancer who have not previously received chemotherapy should be tested for epidermal growth factor receptor (EGFR) mutations.
The recommended dose of Erlotinib-Vista is 150 mg once daily 1 hour before or 2 hours after a meal.
Pancreatic cancer.
The recommended dose of Erlotinib-Vista is 100 mg once daily 1 hour before or 2 hours after food in combination with gemcitabine (see also the instructions for medical use of gemcitabine, indication - pancreatic cancer).
If the patient does not develop a rash within the first 4-8 weeks of treatment, further treatment with Erlotinib should be considered (see section 5.1).
If dose adjustment is necessary, the dose should be reduced in 50 mg steps (see section 4.4). Dose adjustment may be necessary when CYP3A4 substrates and modulators are used concomitantly (see section 4.5).
Liver dysfunction.
Erlotinib is eliminated by hepatic metabolism and is excreted in the bile. Although erlotinib exposure was similar in patients with moderate hepatic impairment (Child-Pugh score 7-9) compared to patients with normal hepatic function, caution should be exercised when using Erlotinib in patients with hepatic impairment. If severe adverse reactions occur, the dose of Erlotinib should be reduced or discontinued.
Specifications
Characteristics
Active ingredient
Erlotinib
Adults
Can
Country of manufacture
Great Britain
Diabetics
With caution
Dosage
100 мг
Drivers
No data on exposure
For allergies
With caution
For children
It is impossible.
Form
Film-coated tablets
Method of application
Inside, solid
Nursing
It is impossible.
Pregnant
It is impossible.
Primary packaging
blister
Producer
Mistral Capital Management
Quantity per package
30 pcs
Trade name
Erlotinib
Vacation conditions
By prescription
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