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Find Clinical Drug Pipeline Developments & Deals by Vincerx Pharma
The net proceeds will be used to develop company's pipeline through preclinical studies, clinical trials and regulatory submissions, including VIP924, a first-in-class CXCR5-targeting ADC, being developed for the treatment of B-cell malignancies.
The net gross proceeds will be utilized to finance the clinical development of VIP236, which is currently undergoing early-stage clinical trials for the treatment of multiple neoplasms.
VIP152 (enitociclib) is a highly selective CDK9 inhibitor that prevents activation of RNA polymerase II, resulting in reduction of known oncogenes MYC and MCL1. It is currently in Phase 1/2 trials combination with venetoclax and prednisone for the treatment of Lymphoma.
VIP943 is a novel ADC developed using Vincerx’s next-generation ADC technology designed to bind with CD123 and is being investigated in acute myeloid leukemia.
VIP943 is a novel ADC developed using Vincerx’s next-generation ADC technology designed to bind with CD123 and is being investigated in acute myeloid leukemia.
VIP236 is a small molecule drug conjugate with an optimized camptothecin payload having a significant activity in patient-derived and metastatic cancer models. It is being developed for treating multiple solid tumors.
VIP236 is a first-in-class SMDC with a tailored design to efficiently treat patients with cancer with aggressive and metastatic disease. VIP236 binds to activated αVβ3 integrin allowing specific homing to the tumor and is efficiently cleaved by neutrophil elastase (NE).
VIP943 is a next-generation ADC with a differentiated safety profile from currently approved ADCs. In vitro and in vivo studies using patient-derived AML cells show VIP943 has favorable monotherapy and combination efficacy including targeting of leukemic stem cells.
Preclinical data demonstrate VIP152 as the most selective CDK9 inhibitor compared with other CDK9 inhibitors, with the most robust MYC mRNA downregulation.
VIP152, a selective CDK9 inhibitor, induces complete regression of high-grade B-cell lymphoma (HGBL) models and depletion of short-lived oncogenic driver transcripts, MYC and MCL1, with a once weekly schedule.
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