DDInter1840 DDInter1479
Trabectedin, also referred as ET-743 during its development, is a marine-derived antitumor agent discovered in the Carribean tunicate _Ecteinascidia turbinata_ and now produced synthetically. Trabectedin has a unique mechanism of action. It binds to the minor groove of DNA interfering with cell division and genetic transcription processes and DNA repair machinery. It is approved for use in Europe, Russia and South Korea for the treatment of advanced soft tissue sarcoma. It is currently under evaluation for the treatment of breast cancer, prostate cancer, in addition to pediatric sarcomas. Both the European Commission and the U.S. Food and Drug Administration (FDA) have approved trabectedin as an orphan drug in soft tissue sarcomas and ovarian cancer. On October 23, 2015, the FDA approved trabectedin, (as Yondelis), for the treatment of specific soft tissue sarcomas.
Pitavastatin, also known as the brand name product Livalo, is a lipid-lowering drug belonging to the statin class of medications. By inhibiting the endogenous production of cholesterol within the liver, statins lower abnormal cholesterol and lipid levels and ultimately reduce the risk of cardiovascular disease. More specifically, statin medications competitively inhibit the enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) Reductase, which catalyzes the conversion of HMG-CoA to mevalonic acid. This is the third step in a sequence of metabolic reactions involved in the production of several compounds involved in lipid metabolism and transport including cholesterol, low-density lipoprotein (LDL) (sometimes referred to as "bad cholesterol"), and very low-density lipoprotein (VLDL). Prescribing of statin medications is considered standard practice following any cardiovascular events and for people with a moderate to high risk of development of CVD, such as those with Type 2 Diabetes. The clear evidence of the benefit of statin use coupled with very minimal side effects or long term effects has resulted in this class becoming one of the most widely prescribed medications in North America.[A181087, A181406] Pitavastatin and other drugs from the statin class of medications including [atorvastatin], [pravastatin], [rosuvastatin], [fluvastatin], and [lovastatin] are considered first-line options for the treatment of dyslipidemia.[A181087, A181406] Increasing use of the statin class of drugs is largely due to the fact that cardiovascular disease (CVD), which includes heart attack, atherosclerosis, angina, peripheral artery disease, and stroke, has become a leading cause of death in high-income countries and a major cause of morbidity around the world. Elevated cholesterol levels, and in particular, elevated low-density lipoprotein (LDL) levels, are an important risk factor for the development of CVD.[A181087,A181553] Use of statins to target and reduce LDL levels has been shown in a number of landmark studies to significantly reduce the risk of development of CVD and all-cause mortality.[A181090,A181093,A181096,A181427,A181475,A181538] Statins are considered a cost-effective treatment option for CVD due to their evidence of reducing all-cause mortality including fatal and non-fatal CVD as well as the need for surgical revascularization or angioplasty following a heart attack.[A181087, A181406] Evidence has shown that even for low-risk individuals (with <10% risk of a major vascular event occurring within 5 years) statins cause a 20%-22% relative reduction in major cardiovascular events (heart attack, stroke, coronary revascularization, and coronary death) for every 1 mmol/L reduction in LDL without any significant side effects or risks.[A181397, A181403] While all statin medications are considered equally effective from a clinical standpoint, [rosuvastatin] is considered the most potent; doses of 10 to 40mg [rosuvastatin] per day were found in clinical studies to result in a 45.8% to 54.6% decrease in LDL cholesterol levels.[A181409,A181535,A181538,A1793] Study data has confirmed that pitavastatin's potency in lowering LDL-C is comparable to that of other statins but also has increased efficacy in increasing HDL-C (also known as "good cholesterol").[A182000,A182003,A182006] Despite these differences in potency, several trials have demonstrated only minimal differences in terms of clinical outcomes between statins.[A181538, A181427]
Trabectedin {u} (Compound) binds {v} (Gene) CYP2C9
CYP2C9 {u} (Gene) is bound by {v} (Compound) Pitavastatin
Trabectedin {u} (Compound) causes {v} (Side Effect) Dermatitis
Dermatitis {u} (Side Effect) is caused by {v} (Compound) Pitavastatin
Trabectedin {u} (Compound) binds {v} (Gene) CYP2C9
CYP2C9 {u} (Gene) is bound by {v} (Compound) Fluvastatin
Fluvastatin {u} (Compound) resembles {v} (Compound) Pitavastatin
Trabectedin {u} (Compound) causes {v} (Side Effect) Dermatitis
Dermatitis {u} (Side Effect) is caused by {v} (Compound) Fluvastatin
Fluvastatin {u} (Compound) resembles {v} (Compound) Pitavastatin
Trabectedin {u} (Compound) binds {v} (Gene) SRC
SRC {u} (Gene) regulates {v} (Gene) CCNA2
CCNA2 {u} (Gene) is downregulated by {v} (Compound) Pitavastatin
Trabectedin {u} (Compound) causes {v} (Side Effect) Jaundice
Jaundice {u} (Side Effect) is caused by {v} (Compound) Etoposide
Etoposide {u} may cause a moderate interaction that could exacerbate diseases when taken with {v} Pitavastatin
Trabectedin {u} (Compound) binds {v} (Gene) CYP2C9
CYP2C9 {u} (Gene) is bound by {v} (Compound) Atorvastatin
Atorvastatin {u} (Compound) resembles {v} (Compound) Pitavastatin
Trabectedin {u} (Compound) binds {v} (Gene) PTGS1
PTGS1 {u} (Gene) is bound by {v} (Compound) Zafirlukast
Zafirlukast {u} may cause a moderate interaction that could exacerbate diseases when taken with {v} Pitavastatin
Trabectedin {u} (Compound) binds {v} (Gene) SRC
SRC {u} (Gene) interacts with {v} (Gene) and {u} (Gene) is regulated by {v} (Gene) FAS
FAS {u} (Gene) is upregulated by {v} (Compound) Pitavastatin
Trabectedin {u} (Compound) binds {v} (Gene) CYP2C9
CYP2C9 {u} (Gene) is bound by {v} (Compound) Warfarin
Warfarin {u} may cause a minor interaction that can limit clinical effects when taken with {v} Pitavastatin
Trabectedin (Compound) binds CYP2C9 (Gene) and CYP2C9 (Gene) is bound by Pitavastatin (Compound)
Trabectedin (Compound) causes Dermatitis (Side Effect) and Dermatitis (Side Effect) is caused by Pitavastatin (Compound)
Trabectedin (Compound) binds CYP2C9 (Gene) and CYP2C9 (Gene) is bound by Fluvastatin (Compound) and Fluvastatin (Compound) resembles Pitavastatin (Compound)
Trabectedin (Compound) causes Dermatitis (Side Effect) and Dermatitis (Side Effect) is caused by Fluvastatin (Compound) and Fluvastatin (Compound) resembles Pitavastatin (Compound)
Trabectedin (Compound) binds SRC (Gene) and SRC (Gene) regulates CCNA2 (Gene) and CCNA2 (Gene) is downregulated by Pitavastatin (Compound)
Trabectedin (Compound) causes Jaundice (Side Effect) and Jaundice (Side Effect) is caused by Etoposide (Compound) and Etoposide may cause a moderate interaction that could exacerbate diseases when taken with Pitavastatin
Trabectedin (Compound) binds CYP2C9 (Gene) and CYP2C9 (Gene) is bound by Atorvastatin (Compound) and Atorvastatin (Compound) resembles Pitavastatin (Compound)
Trabectedin (Compound) binds PTGS1 (Gene) and PTGS1 (Gene) is bound by Zafirlukast (Compound) and Zafirlukast may cause a moderate interaction that could exacerbate diseases when taken with Pitavastatin
Trabectedin (Compound) binds SRC (Gene) and SRC (Gene) interacts with FAS (Gene) and SRC (Gene) is regulated by FAS (Gene) and FAS (Gene) is upregulated by Pitavastatin (Compound)
Trabectedin (Compound) binds CYP2C9 (Gene) and CYP2C9 (Gene) is bound by Warfarin (Compound) and Warfarin may cause a minor interaction that can limit clinical effects when taken with Pitavastatin