Above: Current treatment of multiple myeloma. (A) Newly diagnosed and (B) relapsed. *Or similar bortezomib-based triplet. **Bortezomib may be preferred for intermediate- and high-risk patients. ☨Consider salvage ASCT in patients eligible for ASCT. ➻Any of the regimenslisted for first relapse that the patient has not previously been exposed to. ASCT, autologous stem cell transplantation; DRD, daratumumab, lenalidomide, dexamethasone; DVD, daratumumab, bortezomib, dexamethasone; ERD, elotuzumab, lenalidomide, dexamethasone; IRD, ixazomib, lenalidomide, dexamethasone; KRD, carfilzomib, lenalidomide, dexamethasone; PD, pomalidomide plus dexamethasone. Rd, lenalidomide, dexamethasone; VCD, bortezomib, cyclophosphamide, dexamethasone;VRD, bortezomib, lenalidomide. dexamethasone.
Useful medications:
Therapeutic Suggestions 2016-17:
Triplet induction with VRD that combines a proteasome inhibitor and an immunomodulatory drug improves OS while ASCT improves PFS in the context of modern therapy. Posttransplant maintenance (lenalidomide in standard-risk myeloma and bortezomib in intermediate- and high-risk myeloma) improves OS.
Identification and approval of new effective drugs
• Carfilzomib (irreversible proteasome inhibitor)
• Pomalidomide (new immunomodulatory analog
of lenalidomide)
• Panobinostat (deacetylase inhibitor)
• Elotuzumab (anti-SLAMF7 monoclonal
antibody)
• Daratumumab (anti-CD38 monoclonal antibody)
• Ixazomib (oral proteasome inhibitor)
Identification of investigational drugs with
single-agent activity
• Isatuximab (anti-CD38 monoclonal antibody)
• Marizomib (proteasome inhibitor)
• Oprozomib (oral proteasome inhibitor)
• Filanesib (kinesin spindle protein inhibitor)
• Dinaciclib (cyclin-dependent kinase inhibitor)
• Venetoclax (selective BCL-2 inhibitor)
• LGH-447 (pan PIM1-3 kinase inhibitor)
• Nelfinavir (Proteasome inhibitor used in AIDS)
BCL-2, B-cell lymphoma; OS, overall survival; PFS, progression-free survival; PIM, proto-oncogene serine/threonine-protein; The surface antigen CD 319 (SLAMF7) is a marker of normal and malignant plasma cells in multiple myeloma.
Modified by Glenn Tisman, M.D.