This drug is better preferred than bortezomib due to many of its advantages, such as its more specific and with a small activity outside of the proteasome. Carfilzomib doesn’t become resistance to the tumor cell compared to bortezomib due to this reason this drug was synthesized for better treatment for cancer. The process of this drug is similar to bortezomib in some way, it is capable to delay proliferation and induce apoptosis to malignant plasma cells due to the selectivity and irreversible of the inhibition of proteasomes [27]. The administration for carfilzomib is through intravenous due to the same problem of BTZ, having a low bioavailability. In clinical trials, the dose of 20 mg/m2 is given to all the patients which immediately, scientist …show more content…
The metabolism of carfilzomib consists of two pathways peptidase cleavage and epoxide hydrolysis, that were found in peptide pieces with the diol metabolite in carfilzomib. The drug has a half-life of less than one hour and is excreted by biliary and renal excretion, less than one percent of the drug remains complete [7]. All drugs eventually have severe side effects depending on the type of drug used. This drug, carfilzomib has mostly common side effects such as a cough, diarrhea, hypertension, thrombocytopenia, muscle spasms, upper respiratory tract infection, and hypokalemia, these side effects are not life-threatening, but during clinical trials a 3.8% of the patients were reported with cardiac failure [7]. In further studies, researchers were able to understand that the higher the drug dose caused severe side effects, patients experience cardiovascular adverse events (CVAE) mainly heart failure, heart attacks, and arrhythmia [4]. This side effects can be taken into account that they may depend on the age and obesity of the …show more content…
This can be taken into consideration that patients taking the drug bortezomib for the treatment of multiple myeloma is not effective so the second-generation drug carfilzomib with lenalidomide and desxamethasone can be taken into account that the drug may overcome the bortezomib resistance and treat MM. Lenalidomide is an immunomodulatory drug that is an analogue of thalidomide that possess pleiotropic anti-myeloma properties that include such as anti-angiogenic, anti-inflammatory, and anti-tumor necrosis factor activity [10]. This drug is derived by adding an amigo group to the fourth carbon of the phthaloyl ring of thalidomide [10]. Dexamethasone is a corticosteroid that is an anti-inflammatory medication that also has the ability to treat some types of cancers when its combined with a proteasome inhibitor drug
Gleevec scientifically known as CGP57148 (imatinib) and formerly known as STI571 is the new member of a class of agents that act by binding using a kinase inhibitor to try to control CML. It acts as a specific kinase inhibitor, which induces complete remission in the population of those with chronic-phase CML. As a result of the treatment there are no immature cells seen in the blood, and the spleen returns to its normal size in a complete hematologic response (CHR). Equally patients using Gleevec see a dramatic reduction of their tumor clone cells, and restores normal regulatory behavior in the leukemic clone. As well as, the occurrence of a marked increase in the proportion of blast cells, this in addition leaves cells undamaged. If no cells with the Philadelphia chromosome are found in the blood or bone marrow, then patients obtain a complete cytogenetic response (CCyR).
...6 and Sitagliptin at week 52 (p <0.001). Canagliflozin 100 mg and 300 mg reduced body weight vs placebo (week 26: –3.7%, –4.2%, –1.2%, respectively; p <0.001) and sitagliptin (week 52: –3.8%, –4.2%, –1.3%, respectively; p <0.001). Both canagliflozin doses reduced FPG and systolic BP vs placebo (week 26) and sitagliptin (week 52) (p <0.001).5
Four therapies have been described to decrease the muscle toxicity of doxorubicin. First, use of the iron chelator dexrazoxane decreases muscle toxicity (36, 89).Second, aerobic exercise has been shown to protect against doxorubicin induced skeletal muscle apoptosis through decreasing autophagy signaling (50, 84, 85). Third, the mitochondrial antioxidant SS31 protects against doxorubicin induced apoptosis (32). Fourth, pretreatment of metformin, an anti-diabetic drug, decreases cardiomyocyte apoptosis (7, 8). The interaction of doxorubicin and metformin will be discussed in greater detail in upcoming sections.
The medication has impacted her life enormously. She states that she was unable to function normally and felt physically ill. She was often light headed and nauseated, and her energy levels were low. Now she feels like a new person as she states. She has energy to play with her children and to garden weather permiting.
In today days Atrial Fibrillation (AF) is the most common cardiac dysrhythmia that is often seen in clinical practice. There are 700,000 strokes in the USA each year and 15% of it caused by Atrial Fibrillation. For a long period of time warfarin was the only oral anticoagulant available in the US for patients with atrial fibrillation to prevent stroke events. Recently a new oral anticoagulants, including apixaban, dabigatran, and rivaroxaban have been developed and became available in the US for the stoke prevention and systemic embolism for patients with atrial fibrillation. Now, when all three new anticoagulants are available as an alternative to warfarin for the same indication, they make the health care providers question which agent is the best and for which patients. New agents have practical advantages over warfarin that has many limitations such as need for monitoring, regular dose adjustment, food and drug interaction and side effects. The major goal of the health care providers is to prescribe the safest and the most effective alternative drug and dose to each individual patient with AF. However, the approval for clinical use by the Food and Drug Administration (FDA) and the European Medicine Agency differ for anticoagulants and their dosages, and for the individual indication (Harenberg & Kraemer, 2012). Thus, more research needs to be done regarding the monitoring tools for new anticoagulant agents, and extend the use of these agents to other patient population.
In the naloxegol group, 81.8% of patients experienced an adverse event (AE), 9.6% experienced a serious AE, and 10.5% experienced an AE that resulted in discontinuation of the product. In the usual care group, 72.2% of patients experienced an AE, and 11.1% experienced a serious AE. In this group, patients could switch to a different usual care treatment option at any time during the study, so data for discontinuation due to AE is not applicable. It was determined that there needed to be over 300 patients in the naloxegol group and over 100 patients in the usual care group. Both of these requirements were
...in the United States is ABVD which includes the drugs Adriamycin, Bleomycin, Vinblastine, and Dacarbazine. Other treatments for lymphoma include radiation therapy, monoclonal antibodies, and stem cell transplants. Radiation therapy uses high-energy rays or particles to kill cancer cells. Monoclonal antibodies use cloned antibodies like the immune system does to kill cancer cells. Stem cell transplants are injected to help create other healthy cells that can then be used to help kill cancer.
Chemotherapy is the use of chemicals to cure cancer. Chemotherapy is also known as “chemo”. The term for chemo came from the German bacteriologist Paul Ehrlich around the year 1900. He came up with the term when he was examining aniline dyes and arsenicals as possible treatments for diseases such as syphilis. He envisioned “magic bullets” that would be able to target invading organisms but still leave the host unscathed. This goal has been providing therapeutic benefits without many side effects in all areas of drug development. There has been a lot of success with compounds that modulate normal biochemistry within the body.
Cancer is one of the leading causes of death worldwide as it can develop in almost any organ or tissue. Significant advances in understanding the cellular basis of cancer and the underlying biological mechanisms of tumour has been vastly improved in the recent years (Jiang et al. 1994). Cancer is a genetic disease which requires series of mutation during cell division to develop, it has characteristics which can be associated with their ability to grow and divide abnormal cells uncontrollable while in the mean time invade and cause nearby blood vessels to serve its need. Even though many people are affected by cancer today, the abilities which cancer cells own make it hard to find single effective treatment for cancer. The focus of research now lies on developing drugs which target cancer cells in the hope to cure cancer once and for all.
Chemotherapy is the use of chemotherapeutic agents to treat cancers. Chemotherapy for stage IV melanoma patients is ineffective, and only yields responses of 10-20% (Anderson, Buzaid and Legha, 1995). Single-agent chemotherapy, Dacarbazine, is the only Food and Drug Administration (FDA) approved chemotherapeutic agent for treatment of metastatic melanoma. The response rate is approximately 15% at initial treatment, however the effects are not long lasting, at less than 2% survival at 6 years. Combination chemotherapy shows slightly higher response rates compared to single-agent chemotherapy, and remission rates are slightly improved (Bhatia, Tykodi, and Thompson,
In one study, there was a reduction in ulcer diameter in 90% of patients treated with thalidomide at an initial oral dose of 400mg/d for 1 week, followed by 200mg/d for 7 weeks [11]. In another study, cachexic patients who received 400mg/d of thalidomide had significant weight gain and/or no progression of wasting [12]. The effect of thalidomide in cachexia may be due to its role in the reduction of cytokines that are mediators of this condition [23]. Although thalidomide has demonstrated an undeniable benefit in the treatment of ENL, malignant tumours, and HIV-linked oral ulcers and wasting syndrome, caution must be taken given the frequent occurrence of side effects, such as teratogenesis, and many CNS
Both these cell lines are known to express endogenous transporters (39) and results from these studies should be interpreted with caution. When uptake studies were done in LLC-PK1 wild type cells, dasatinib intracellular concentrations were found to be significantly increased in the presence of 50μM pazopanib and regorafenib. LLC-PK1 cells express endogenous BCRP and pazopanib and regorafenib were found to be significant BCRP inhibitors in our earlier uptake study with MDCK-II-BCRP cells. Therefore, it is likely that these endogenous BCRP transporters maybe responsible for the uptake change observed. Further, dasatinib intracellular concentrations significantly decreased in the presence of afatinib, bosutinib, gefitinib, imatinib, lapatinib, ponatinib, sunitinib and vandetanib. LLC-PK1 cells do not express OATP-C uptake transporters.(40) Dasatinib uptake studies in MDCK-II wild type cells revealed a slightly different trend. Among the 14 ingredients screened, 6 of them, namely, axitinib, erlotinib, imatinib, lapatinib, nilotinib and pazopanib exhibited a significant increase in dasatinib intracellular concentrations. MDCK-II cells have very little BCRP expression but have endogenous Pgp expression. Since axitinib, imatinib, lapatinib, nilotinib and pazopanib showed potent Pgp inhibition in the uptake study conducted in LLC-PK1-Pgp cells, the increased dasatinib uptake in MDCK-II wild
Disease modifying anti rheumatic drugs are a class of medication commonly used to slow down the progression of the disease. DMARDs work by altering the genetic makeup and suppressing the body’s immune system. Dependi...
is an international confederation of 17 different organisations working in 94 countries worldwide to find solution for the poverty, so it is also owned by many people.
Pre-discovery process is the first stage of drug discovery. During Pre-discovery stage chemists and pharmacologists endeavor to understand and identify the factors which can play a significant role in the particular disease. After revealing the cause of disease or understanding it a target molecule against which drug will act is being chosen. In order to understand the structure the target molecule is eliminated, isolated and its various interactions are inquired. Understanding interactions of the molecule can be helpful in finding treatment of a specific disease. Next stage includes the demonstration that the chosen molecule is relevant to the disease and proof that the drug target is associated with a desired change in the behavior of diseased cells (PPD, 2011).