Neuroendocrine tumors (NET) are a heterogeneous group of neoplasms, arising from cells of the endocrine system, with varying clinical behaviors. Although these neoplasms are considered rare, a significant increase in the incidence and detectability of NET has been noted in many epidemiological studies in recent years.^1-4  Currently, the new pathologic classification of NEN is based on UICC/AJCC, divided NEN into well differentiated neuroendocrine tumors (NET) NET G1 (Ki-67 < 3%), G2 (Ki-67 3%-20%) and G3 (Ki-67 21%-55%), and poor differentiated neuroendocrine carcinoma(NEC) (Ki-67 > 20%). ⁵Somatostatin receptor directed Peptide receptor radiotherapy (PRRT) with β-particle emitter ¹⁷⁷Lu-DOTATATE is currently one of the more effective therapies for well differentiated gastroenteropancreatic NETs.  PRRT is fairly well tolerated without any severe adverse effects  and  has been shown to improve survival parameters. The first open, randomized, controlled trial : the NETTER-1 trial demonstrated significantly improved PFS with ¹⁷⁷Lu-DOTATATE as compared to Octreotide LAR (Sandostatin LAR; 60 mg) (PFS 40 months vs 8.4 months) in patients with advanced midgut NET⁶. Various other trials have shown the superiority of PRRT in improving survival advantage compared to other forms of treatment including targeted therapy with mTOR or kinase inhibitor. While the results of the NETTER -1 trial led to the approval of Lu-177 DOTATATE therapy by the US FDA, PRRT with Lu177 DOTATATE has been practiced in the European countries, Australia and India for more than 25 years.PRRT with β-emitters has a good clinical effect, However, the relatively large penetration range of the β particle does result in some collateral damage to surrounding normal tissue especially the bone marrow in patients of bone metastases and normal liver parenchyma in cases of extensive hepatic metastases. The dose limits for non target tissue often limits the number of cycles of PRRT possible to a patient for the treatment of the disease.  Also, due to hypoxia cancer tissue could be resistant for β-emitters treatment. Radioisotopes emitting α-particles which have higher energy and shorter penetration range in comparison to β-particles have distinct advantages for use in targeted therapy.α-particles with high linear energy transfer (LET ≈100 keV/µm) give the higher probability of double strand breaks compared with β-particles with low LET (probability of double strand break increase ∼20 times). On the other hand, the short range (<100 µm) of α-particles in human tissue resulted in minimizing damage to surrounding healthy tissue.⁷ Cell death induced by α-radiation is predominantly due to DNA double strand breaks and induced apoptosis so it is largely independent of cell cycle phase and cell oxygenation status.⁸Due to problems of availability and production, half-life, cost and the ability to chemically and stably incorporate them into a suitable vector, only a few of α-radionuclides are medically relevant and available for potential clinical use. These include ²¹¹At, ²¹²Bi, ²¹³Bi, ²²⁵Ac, ²²³Ra, ²¹²Pb, ²²⁷Th, and ¹⁴⁹Tb.^8 212Pb is of definite interest because its daughter nuclides (212Bi and 212Po) undergo α-decay, which allows us to view ²¹²Pb as an in-vivo generator of α-particles emitters. Also, Lead-212, with a convenient half-life of 10.64 h, and daughter alpha-emitter short-lived ²¹²Bi (T1/2 = 1 h), provides the possibility for the synthesis and purification of complex radiopharmaceuticals with minimum loss of radioactivity during preparation⁹. As a benefit for clinical implementation, it can be milked from a radionuclide generator in different ways. Because ²¹²Pb is an in-vivo generator of alpha particles, it is particularly suitable for SSTR therapy applications. VMT-α-peptide is a modified somatostatin receptor targeted peptide with improved pharmacokinetics and chelation of ²⁰³Pb/²¹²Pb. ²¹²Pb-VMT-α-peptide is a radio-therapeutic drug indicated in subjects with unresectable, metastatic somatostatin receptor (SSTR) positive neuroendocrine tumors (NETs)¹⁰. The VMT chelator efficiently chelates ²¹²Pb as well as its daughter ²¹²Bi. Short half-lives of ²¹²Bi daughters ²⁰⁸Tl and ²¹²Po (3 min and 0.3 µs respectively) and strong chelation properties of the VMT-α-NET ensures that α-particles in the decay series are mainly emitted in the target tissue. This drug addresses an unmet need in the field of peptide receptor radionuclide therapy (PRRT) for NETs.The current study is an open ended pilot study to evaluate the safety & clinical efficacy of targeted alpha therapy with 212Pb-VMT-α-peptide and will help in clinical translation of alpha PRRT with Pb212 in patients of metastatic Somatostatin Receptor Expressing Neuroendocrine Tumors.