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This drug has a boxed warning. This is the most serious warning from the Food and Drug Administration (FDA). A boxed warning alerts doctors and patients about drug effects that may be dangerous.
- This drug may increase your liver enzymes. This can lead to liver damage. Your doctor will check your liver function when you first start taking this drug and during treatment. If your liver isn’t working well, your doctor may lower your dosage or stop your treatment with this drug.
- Eltrombopag oral tablet is available as a brand-name drug. It’s not available as a generic drug. Brand name: Promacta.
- Eltrombopag comes in two forms: oral tablet and oral suspension.
- Eltrombopag oral tablet is used to treat low platelet levels due to chronic immune thrombocytopenia (ITP) or chronic hepatitis C virus infection. It’s also used to treat severe aplastic anaemia.
Eltrombopag is a prescription drug. It comes as an oral tablet and an oral suspension.
Eltrombopag oral tablet is available as the brand-name drug Promacta. It’s not available as a generic drug.
This drug may be used as part of combination therapy. This means you may need to take it with other medications.
Why it’s used
Eltrombopag is used to treat:
- Low platelet levels due to chronic immune thrombocytopenia (ITP). This is a bleeding disorder. Eltrombopag is given to people who haven’t responded well to other drugs or surgery.
- Low platelet counts due to chronic hepatitis C virus infection. This drug is used before and during treatment with the drug pegylated interferon and ribavirin.
- Severe aplastic anemia. Aplastic anaemia is when you have bone marrow failure, which results in low levels of platelets, red blood cells, and white blood cells. Eltrombopag is used in two ways for this condition:
- First-line treatment of severe aplastic anaemia. This drug can be used as the first treatment option in some cases of severe aplastic anaemia. For this use, eltrombopag is given in combination with other initial treatments.
- Treatment of refractory severe aplastic anaemia. Some cases of severe aplastic anaemia are refractory, which means the anaemia did not improve after treatment with other medications. Eltrombopag can be used alone for treating these cases of anaemia.
Eltrombopag is not used to treat myelodysplastic syndrome (MDS).
How it works
Eltrombopag belongs to a class of drugs called thrombopoietin (TPO) receptor agonists. A class of drugs is a group of medications that work similarly. These drugs are often used to treat similar conditions.
Eltrombopag works by increasing cells in your bone marrow. It causes these cells to make more platelets. This effect lowers your risk of bleeding.
Osicent 80: Each tablet contains Osimertinib Mesylate INN equivalent to Osimertinib 80 mg.
Osimertinib is a kinase inhibitor of the epidermal growth factor receptor (EGFR), which binds irreversibly to certain mutant forms of EGFR (T790M, L858R, and exon 19 deletions) at approximately 9-fold lower concentrations than wild-type. In cultured cells and animal tumour implantation models, osimertinib exhibited anti-tumour activity against non-small cell lung cancer (NSCLC) lines harbouring EGFR-mutations (T790M/L858R, L858R, T790M/exon 19 deletion, and exon 19 deletions) and, to a lesser extent, wild-type EGFR amplifications.
Osimertinib is a kinase inhibitor indicated for the treatment of patients with metastatic epidermal growth factor receptor (EGFR) T790M mutation-positive non-small cell lung cancer (NSCLC), as detected by an FDA-approved test, who have progressed on or after EGFR tyrosine kinase inhibitor therapy.
Dosage & Administration
80 mg orally once daily, with or without food.
The most common (>20%) adverse reactions (all grades) observed in Osimertinib-treated patients were diarrhoea (42%), rash (41%), dry skin (31%), and nail toxicity (25%). The most frequent adverse reactions that led to dose reductions or interruptions were: electrocardiogram QTc prolonged (2.2%) and neutropenia (1.9%). Serious adverse reactions reported in 2% or more patients were pneumonia and pulmonary embolus.
Interstitial Lung Disease (ILD)/Pneumonitis: Occurred in 3.3% of patients. Osimertinib should be permanently discontinued in patients diagnosed with ILD/Pneumonitis.
QTc Interval Prolongation: Electrocardiograms and electrolytes should be monitored in patients who have a history or predisposition for QTc prolongation, or those who are taking medications that are known to prolong the QTc interval. Osimertinib should be withheld then restarted at a reduced dose or permanently discontinued.
Cardiomyopathy: Occurred in 1.4% of patients. Left ventricular ejection fraction (LVEF) should be assessed before treatment and then every 3 months thereafter.
Embryo-Fetal Toxicity: Osimertinib can cause fetal harm. Females should be advised of the potential risk to the fetus and to use effective contraception during treatment with Osimertinib and for 6 weeks after the final dose. Males should be advised to use effective contraception for 4 months, after the last dose of Osimertinib.
Use in Pregnancy & Lactation
Based on its mechanism of action and animal data, Osimertinib can cause fetal harm when administered to a pregnant woman. There are no available data on Osimertinib use in pregnant women. Pregnant women should be advised of the potential risk to a fetus.
There are no data on the presence of Osimertinib in human milk, the effects of Osimertinib on the breastfed infant or on milk production. A lactating woman should be advised not to breastfeed during treatment.
The safety and effectiveness of Osimertinib in pediatric patients have not been established.
No overall differences in safety were observed between patients 65 years and older and those younger than 65 years.
Strong CYP3A Inhibitors
Concomitant administration of Osimertinib should be avoided with strong CYP3A inhibitors, including macrolide antibiotics (e.g., telithromycin), antifungals (e.g., itraconazole), antivirals (e.g., ritonavir), nefazodone, as concomitant use of strong CYP3A inhibitors may increase Osimertinib plasma concentrations. If no other alternative exists, patients should be monitored more closely for adverse reactions.
Strong CYP3A Inducers
Concomitant administration of Osimertinib should be avoided with strong CYP3A inducers (e.g., phenytoin, rifampicin, carbamazepine, St. John’s Wort) as strong CYP3A inducers may decrease Osimertinib plasma concentrations.
Osicent 80 Container Pack: Each bottle contains 30 tablets.
Osicent 80: Each box contains 1 blister strip of 10 tablets.
Panovir: Each tablet contains Sofosbuvir INN 400 mg and Velpatasvir INN 100 mg.
It is a fixed-dose combination tablet containing sofosbuvir and velpatasvir for oral administration. Sofosbuvir is a nucleotide analogue HCV NS5B polymerase inhibitor and velpatasvir is an NS5A inhibitor.
Sofosbuvir and Velpatasvir combination is indicated for the treatment of adult patients with chronic hepatitis C virus (HCV) genotype 1, 2, 3, 4, 5 or 6 infection
– without cirrhosis or with compensated cirrhosis
– with decompensated cirrhosis for use in combination with ribavirin
Dosage & Administration
The recommended dosage is one tablet (400 mg of Sofosbuvir and 100 mg of Velpatasvir) taken orally once daily. Recommended treatment regimen:
– Patients without cirrhosis and patients with compensated cirrhosis (Child-Pugh A) – one tablet once daily for 12 weeks
– Patients with decompensated cirrhosis (Child-Pugh B or C) – one tablet once daily and Ribavirin for 12 weeks. The recommended dosage of Ribavirin is based on body weight (1000 mg/day for patients < 75 kg and 1200 mg/day for ≥ 75 kg, in two divided doses/day)
No dosage recommendation can be given for patients with severe renal impairment (eGFR ≤ 30 mL/min/1.73 m2) or with ESRD, due to higher exposures of the predominant sofosbuvir metabolite.
The most common side effects of the Sofosbuvir and Velpatasvir combination include headache and tiredness. Treatment may result in slowing of the heart rate along with other symptoms when taken with amiodarone (a medicine used to treat certain heart problems).
Serious symptomatic bradycardia may occur in patients taking amiodarone, particularly in patients also receiving beta-blockers, or those with underlying cardiac comorbidities and/or advanced liver disease. Coadministration of amiodarone with Sofosbuvir and Velpatasvir combination is not recommended. In patients without alternative viable treatment options, cardiac monitoring is recommended.
Use in Pregnancy & Lactation
No adequate human data are available to establish whether or not Sofosbuvir and Velpatasvir combination poses a risk to pregnancy outcomes. If Sofosbuvir and Velpatasvir combination administered with Ribavirin, the combination regimen is contraindicated in pregnant women and in men whose female partner is pregnant or going to be pregnant in the next six months.
Drugs may decrease the concentrations of sofosbuvir and/or velpatasvir: Antacids, H2-receptor antagonists, Proton-pump inhibitors etc.
Coadministration is not recommended with: topotecan, Carbamazepine, Phenytoin, Phenobarbital, Oxcarbazepine, Rifabutin, Rifampin, Rifapentine, efavirenz, Tipranavir, Ritonavir, Hypericum perforatum.
Coadministration of Sofosbuvir and Velpatasvir combination, with Rosuvastatin, Atorvastatin may significantly increase the concentration of Rosuvastatin, Atorvastatin.
If an overdose occurs the patient must be monitored for evidence of toxicity. Treatment of overdose includes monitoring of vital signs as well as observation of the clinical status of the patient.
Store in a cool and dry place (preferably below 30°C). Keep out of reach of children.
Panovir Container Pack: Each bottle contains 28 tablets.
Hanover : Each box contains 1 blister strip of 6 tablets.
Tofacent 5: Each tablet contains Tofacitinib Citrate INN equivalent to Tofacitinib 5 mg
Tofacent XR 11: Each Extended-Release tablet contains Tofacitinib Citrate INN equivalent to Tofacitinib 11 mg
Tofacitinib is a Janus kinase (JAK) inhibitor. JAKs are intracellular enzymes that transmit signals arising from cytokine or growth factor-receptor interactions on the cellular membrane to influence cellular processes of hematopoiesis and immune cell function. Within the signalling pathway, JAKs phosphorylate and activate Signal Transducers and Activators of Transcription (STATs) which modulate intracellular activity including gene expression. Tofacitinib modulates the signalling pathway at the point of JAKs, preventing the phosphorylation and activation of STATs. JAK enzymes transmit cytokine signalling through the pairing of JAKs (e.g., JAK1/JAK3, JAK1/JAK2, JAK1/TyK2 and JAK2/JAK2). Tofacitinib inhibited the in vitro activities of JAK1/JAK2, JAK1/JAK3, and JAK2/JAK2 combinations with IC50 of 406, 56, and 1377 nM, respectively. However, the relevance of specific JAK combinations to therapeutic effectiveness is not known.
Tofacitinib / Tofacitinib XR is a Janus kinase (JAK) inhibitor.
• Rheumatoid Arthritis: Tofacitinib / Tofacitinib XR is indicated for the treatment of adult patients with moderately to severely active
rheumatoid arthritis who have had an inadequate response or intolerance to methotrexate. It may be used as monotherapy or in
combination with methotrexate or other nonbiologic disease-modifying antirheumatic drugs (DMARDs).
• Psoriatic Arthritis: Tofacitinib / Tofacitinib XR is indicated for the treatment of adult patients with active psoriatic arthritis who have
had an inadequate response or intolerance to methotrexate or other disease-modifying antirheumatic drugs (DMARDs).
• Ulcerative Colitis: Tofacitinib is indicated for the treatment of adult patients with moderately to severely active ulcerative colitis (UC).
• Limitations of Use: Use of Tofacitinib / Tofacitinib XR in combination with biologic DMARDs or potent immunosuppressants such as
azathioprine and cyclosporine are not recommended.
Dosage & Administration
Do not initiate Tofacitinib / Tofacitinib XR if absolute lymphocyte count <500 cells/mm3
, an absolute neutrophil count (ANC) <1000
or hemoglobin <9 g/dL.
• Rheumatoid Arthritis: Tofacitinib 5 mg twice daily or Tofacitinib XR 11 mg once daily. Recommended dosage in patients with
moderate and severe renal impairment or moderate hepatic impairment is Tofacitinib 5 mg once daily.
• Psoriatic Arthritis (in combination with nonbiologic DMARDs): Tofacitinib 5 mg twice daily or Tofacitinib XR 11 mg once daily.
Recommended dosage in patients with moderate and severe renal impairment or moderate hepatic impairment is Tofacitinib 5 mg once daily.
• Ulcerative Colitis: • Induction: Tofacitinib 10 mg twice daily or Tofacitinib XR 22 mg once daily for 8 weeks; evaluate patients and
transition to maintenance therapy depending on therapeutic response. If needed, continue Tofacitinib 10 mg twice daily or Tofacitinib
XR 22 mg once daily for a maximum of 16 weeks. Discontinue Tofacitinib 10 mg twice daily or Tofacitinib XR 22 mg once daily after
16 weeks if the adequate therapeutic response is not achieved. • Maintenance: Tofacitinib 5 mg twice daily or Tofacitinib XR 11 mg once
daily. For patients with loss of response during maintenance treatment, Tofacitinib 10 mg twice daily or Tofacitinib XR 22 mg once
daily may be considered and limited to the shortest duration, with careful consideration of the benefits and risks for the individual
patient. Use the lowest effective dose needed to maintain response. • Dosage adjustment is needed in patients with moderate and
severe renal impairment or moderate hepatic impairment.
The most common adverse reactions are:
• Rheumatoid and Psoriatic Arthritis: Reported during the first 3 months in rheumatoid arthritis controlled clinical trials and occurring in
≥2% of patients treated with Tofacitinib monotherapy or in combination with DMARDs: upper respiratory tract infection,
nasopharyngitis, diarrhoea, and headache.
• Ulcerative Colitis: Reported in ≥5% of patients treated with either 5 mg or 10 mg twice daily of Tofacitinib and ≥1% greater than
reported in patients receiving placebo in either the induction or maintenance clinical trials: nasopharyngitis elevated cholesterol
levels, headache, upper respiratory tract infection, increased blood creatine phosphokinase, rash, diarrhoea, and herpes zoster.
• Serious Infections: Use of Tofacitinib / Tofacitinib XR should be avoided during an active serious infection, including localized infections.
• Gastrointestinal Perforations: Caution should be used in patients that may be at increased risk.
• Laboratory Monitoring: Laboratory Monitoring should be recommended due to potential changes in lymphocytes, neutrophils,
haemoglobin, liver enzymes and lipids.
• Immunizations: Live vaccines: Use with Tofacitinib / Tofacitinib XR should be avoided.
Use in Pregnancy & Lactation
Pregnancy Category C. There are no adequate and well-controlled studies in pregnant women. Tofacitinib should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. It is not known whether Tofacitinib is excreted in human milk. Because many drugs are excreted in human milk and because of the potential for serious adverse reactions in nursing infants from Tofacitinib, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug for the mother. Pediatric Use: The safety and effectiveness of Tofacitinib in pediatric patients have not been established. Geriatric Use: The frequency of serious infection among Tofacitinib-treated subjects 65 years of age and older was higher than among those under the age of 65. As there is a higher incidence of infections in the elderly population in general, caution should be used when treating the elderly.
Strong CP3A4 Inhibitors (e.g., ketoconazole): Dosage adjustment of Tofacitinib / Tofacitinib XR is recommended.
Moderate CYP3A4 Inhibitors Coadministered with Strong CYP2C19 Inhibitors (e.g., fluconazole): Dosage adjustment of Tofacitinib /
Tofacitinib XR is recommended.
Strong CYP3A4 Inducers (e.g., rifampin): Coadministration with Tofacitinib / Tofacitinib XR is not recommended.
Immunosuppressive drugs (e.g., azathioprine, tacrolimus, and cyclosporine): Coadministration with Tofacitinib / Tofacitinib XR is not
Do not store above 30 0C. Keep away from light and out of the reach of children.
Tofacent 5: Each box contains 2 blister strips of 10 tablets.
Tofacent XR 11 Container Pack: Each bottle contains 10 tablets.
The words we use in our communication with others, either verbally or in writing, may substantially affect the message being delivered. Of course, what is heard by the receiving party may not necessarily be identical to what we intend to convey. When one is dealing with the topic of cancer, its treatment and consequences, language that clinicians and members of the cancer research community use may have an even greater impact.
During 40 years of working in the oncology arena, I have witnessed the effects of certain words and terms commonly employed within the professional establishment whose unclear meaning and implications for patients, their families, and the general public may not have been adequately considered. Further, they may have resulted in unfortunate confusion rather than enlightenment. The following commentary highlights my perspective on several of these terms.
To palliate, “to make a disease or symptoms less severe or unpleasant without removing the cause” as defined in one English-language dictionary, is a critical goal of medicine, particularly for clinicians dealing with the manifestations of malignant disease. Critically, there is nothing in this definition that speaks to advanced, progressive, incurable, or end-stage illness. The term simply implies a specific therapeutic focus on directly controlling clinically meaningful symptoms, such as administering effective pain medications, rather than a more indirect effect resulting from the rapid or longer-term successful treatment of cancer. This could include, for example, alleviating abdominal pain from the reduction of peritoneal carcinomatosis in response to cytotoxic drug delivery. Although such strategies have become increasingly relevant in cancer management, the term palliative care or, more specifically, a clinical palliative care service, has become essentially synonymous to many patients and their families with end-of-life care. It is not uncommon for patients with cancer to initially decline the opportunity to benefit from the expertise of a first-class palliative care team simply because they assume that this focus on symptom management is inconsistent with the goal of maximizing efforts to prolong survival. As a result, a strong argument can be made to educate both the public and our own clinical colleagues that, although optimal palliation of symptoms is essential when providing end-of-life care, this specific focus and expertise has the potential to be beneficial to patients throughout their cancer journey.
COMPLEMENTARY ALTERNATIVE MEDICINE
It is difficult to identify a clinically related concept that is more inaccurate, distorted, misleading, and potentially dangerous than that of complementary and alternative medicine (CAM). Complementary, or the more appropriate term used today—integrative—clearly implies the use of a wide variety of approaches designed to optimize the quality of life and enhance symptom management during the course of standard antineoplastic therapy. These strategies range from spiritual and behavioural medical support to far less fully understood interventions, such as acupuncture. The critical point here is that there is nothing “alternative” about such interventions because in this model of care they simply do not substitute for known effective anticancer therapeutics. Lumping these completely different concepts together in the expression CAM delivers an inappropriate message regarding the medically legitimate goals of integrative oncology care. Take, for example, one rather bizarre report that appeared in a peer-reviewed journal several years ago. Investigators examined records in the National Cancer Database of 1,901,815 patients treated from January 1, 2004, through December 31, 2013, and identified individuals “who received complementary medicine,” as self-reported by 258 patients, or 0.01% of the total population in this database. The authors concluded that these patients were more likely to refuse conventional cancer treatment and experience inferior survival compared with those who did not list an interest in this approach to cancer care.1 In addition to the profoundly inadequate sample size for drawing any meaningful conclusions, the authors’ decision to consider individuals interested in alternative approaches to conventional therapy as being equivalent to those desiring an integrative strategy focused on enhancing the quality of life while undergoing state-of-the-art oncology care either unintentionally or intentionally distorts facts. The term CAM simply needs to be discarded, never again to be used by cancer specialists, other clinicians, or members of the research community.
PRECISION CANCER MEDICINE
As relevant as the term precision cancer medicine has become in describing a focus of modern anti-neoplastic drug delivery, there remains a serious issue with the way in which many in the oncology community are using it. Precision cancer medicine refers to a specific goal of our treatment paradigm: to become ever more precise in favourably impacting cancer-relevant molecular targets, measured by improved objective response rates, time to disease progression, or overall survival. The term does not refer to a specific time or event, such that one can declare treatment has achieved a state of being optimally “precise.” The fact that a particular trial of a theorized relevant drug-target combination has failed to reveal the benefits of that approach does not signify a failure of the process of precision cancer medicine. Rather, this outcome serves as an example of how the process should work, discarding approaches that have not demonstrated meaningful benefit while continuing to examine other novel strategies that will hopefully, following appropriate clinical investigation, achieve the desired goal.
There is probably a no more powerful word in all of oncology, and no potential question associated with more fear following the diagnosis of cancer, than when a patient or family member inquires: “Will I or my loved one be cured?” Of course, as all oncologists know, the answer to this question can be quite complex, depending on the tumour type, disease stage, and other considerations. The point here is that even when “cure” is a realistic—or at least not irrational—goal of therapy, achieving this clinical state, with important exceptions such as non-melanoma skin cancers, is something one only knows with reasonable medical certainty at some point in the future. Depending on the natural history of the specific malignancy in question, this may represent a period of many years into that future. Providing an honest but also encouraging and hopeful response is one of the first important challenges facing treating oncologists as they begin to assist patients through their cancer survivorship journey.