DDInter1840 DDInter1270
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.
Naxitamab (humanized 3F8, hu3F8) is an IgG1 monoclonal antibody directed against the oncofetal differentiation antigen GD2 disialoganglioside.[L24454,A224604] Normally expressed during fetal development and in mature neurons, pain fibers, and skin cells, GD2 constitutes a highly efficient target in the treatment of neuroblastoma - it is widely expressed across and within neuroblastomas (and other neuroectodermal tumors), and is rarely subject to antigen loss. The first anti-GD2-monoclonal IgG antibody to be approved by the FDA for the treatment of neuroblastoma was [dinutuximab] under the brand name Unituxin in 2015. One stark disadvantage of this therapy is the requirement for concurrent use of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA). Naxitamab-gqgk (Danyelza) was granted accelerated approval by the FDA in November 2020 for the treatment of high-risk relapsed/refractory neuroblastoma of the bone or bone marrow. This approval requires naxitamab to be co-administered only with GM-CSF, a factor known to enhance the granulocyte-mediated antibody-dependent cytotoxicity of anti-GD2 therapies, making the administration of naxitamab therapy markedly simpler than that of its predecessor.
Trabectedin {u} (Compound) binds {v} (Gene) CYP2C9
CYP2C9 {u} (Gene) is bound by {v} (Compound) Ifosfamide
Ifosfamide {u} may cause a moderate interaction that could exacerbate diseases when taken with {v} Naxitamab
Trabectedin {u} (Compound) is included by {v} (Pharmacologic Class) Alkylating Activity
Alkylating Activity {u} (Pharmacologic Class) includes {v} (Compound) Ifosfamide
Ifosfamide {u} may cause a moderate interaction that could exacerbate diseases when taken with {v} Naxitamab
Trabectedin {u} (Compound) causes {v} (Side Effect) Anorexia
Anorexia {u} (Side Effect) is caused by {v} (Compound) Ifosfamide
Ifosfamide {u} may cause a moderate interaction that could exacerbate diseases when taken with {v} Naxitamab
Trabectedin {u} (Compound) binds {v} (Gene) SRC
SRC {u} (Gene) is upregulated by {v} (Compound) Dapsone
Dapsone {u} may cause a moderate interaction that could exacerbate diseases when taken with {v} Naxitamab
Trabectedin {u} (Compound) binds {v} (Gene) SRC
SRC {u} (Gene) is bound by {v} (Compound) and {u} (Gene) is upregulated by {v} (Compound) Crizotinib
Crizotinib {u} may cause a moderate interaction that could exacerbate diseases when taken with {v} Naxitamab
Trabectedin {u} (Compound) binds {v} (Gene) CYP2E1
CYP2E1 {u} (Gene) is bound by {v} (Compound) Fingolimod
Fingolimod {u} may lead to a major life threatening interaction when taken with {v} Naxitamab
Trabectedin {u} (Compound) causes {v} (Side Effect) Alanine aminotransferase increased
Alanine aminotransferase increased {u} (Side Effect) is caused by {v} (Compound) Fingolimod
Fingolimod {u} may lead to a major life threatening interaction when taken with {v} Naxitamab
Trabectedin (Compound) binds CYP2C9 (Gene) and CYP2C9 (Gene) is bound by Ifosfamide (Compound) and Ifosfamide may cause a moderate interaction that could exacerbate diseases when taken with Naxitamab
Trabectedin (Compound) is included by Alkylating Activity (Pharmacologic Class) and Alkylating Activity (Pharmacologic Class) includes Ifosfamide (Compound) and Ifosfamide may cause a moderate interaction that could exacerbate diseases when taken with Naxitamab
Trabectedin (Compound) causes Anorexia (Side Effect) and Anorexia (Side Effect) is caused by Ifosfamide (Compound) and Ifosfamide may cause a moderate interaction that could exacerbate diseases when taken with Naxitamab
Trabectedin (Compound) binds SRC (Gene) and SRC (Gene) is upregulated by Dapsone (Compound) and Dapsone may cause a moderate interaction that could exacerbate diseases when taken with Naxitamab
Trabectedin (Compound) binds SRC (Gene) and SRC (Gene) is bound by Crizotinib (Compound) and SRC (Gene) is upregulated by Crizotinib (Compound) and Crizotinib may cause a moderate interaction that could exacerbate diseases when taken with Naxitamab
Trabectedin (Compound) binds CYP2E1 (Gene) and CYP2E1 (Gene) is bound by Fingolimod (Compound) and Fingolimod may lead to a major life threatening interaction when taken with Naxitamab
Trabectedin (Compound) causes Alanine aminotransferase increased (Side Effect) and Alanine aminotransferase increased (Side Effect) is caused by Fingolimod (Compound) and Fingolimod may lead to a major life threatening interaction when taken with Naxitamab