Somatostatin type 2 receptor (SSTR2) and Cholecystokinin 2 receptor (CCK2R) are GPCRs that are aberrantly regulated in various tumors. It has been well established that SSTR2 is highly and broadly overexpressed in certain neuroendocrine tumors (NETs). Synthetic molecules that mimic the native SSTR2 ligand, somatostatin, have been successfully developed and approved as a theranostic-therapuetic pair, (Netspot® (68Ga-DOTATATE) and Lutathera® (177Lu-DOTATATE), for detecting and treating gastroenteropancreatic neuroendocrine tumors (GEP-NETs). In addition, SSTR2 is also overexpressed in small cell lung cancer (SCLC) as well as medullary thyroid carcinoma (MTC) and SSTR2-targeted radiotherapy has shown promise for the treatment of both cancers. However, the level and breadth of clinical activity leaves room for improvement to address unmet medical need. Like SSTR2, CCK2R is overexpressed in SCLC, MTC and certain NETs and 177Lu-PP-F11N, an analog of the native ligand of CCK2R, has demonstrated specific and high tumor uptake in MTC patients. Importantly, SSTR2 and CCK2R are overexpressed in a complementarily and/or overlapping manner in SCLC, MTC and NETs tumors. This provides rationale for dual-targeting with a SSTR2/CCK2R therapeutic. Using our dual-targeting vector, FL-031, we aim to address the high unmet medical need in patients with SCLC, advanced MTC and NETs whose tumors are SSTR2-negative/low and are resistant or refractory to Lutathera®.