**Abstract**

Multiple Myeloma (MM) is characterized by the abberant proliferation and expansion of plasma cells in the Bone marrow. Despite the broad use of proteasome inhibitors and IMiDs, Multiple Myeloma remains an incurable disease. The introduction of Monoclonal antibodies, along with bi-specific antibodies and check point inhibitors, has significantly enhanced the armamentarium of available therapeutic options in the relapsed setting. The incorporation of the abovementioned novel agents in triplet or quadruplet therapeutic regimens has led to significant prolongation of overall survival (OS) and progression free survival (PFS), without adding significant toxicity. Anti-CD38 monoclonal antibodies has become the cornerstone of antimyeloma therapy in both the newly diagnosed and relapsed setting.

**Keywords:** Monoclonal Antibodies, Antibody Drug Conjugates, Daratumumab, Belantamab Mafodotin

### **1. Introduction**

Multiple Myeloma is characterized by the upregulation and expansion of plasma cells malignant clones in the bone marrow [1]. The introduction of novel agents such as immunomodulatory drugs (IMiDs) and proteasome inhibitors (PIs) has led to significant improvement of disease prognosis and survival. However, the disease remains incurable, and all patients will relapse. Patients who are refractory to both Imids and PIs have poor survival outcomes, with a median overall survival of 9–13 months [2, 3]. The identification of novel therapeutic approaches for this group of patients represents an unmet medical need. In addition to that, patients with advanced disease characteristics and high-risk cytogenetics have a poor prognosis [4, 5]. Immune dysregulation represents a hallmark of MM pathophysiology. A better understanding of mechanisms that govern immune impairment in MM, has led to the development of several immunotherapeutic agents such as monoclonal antibodies, bispecific antibodies (BiTEs), and chimeric antigen receptor (CAR) T-cells.
