LAE001 is a first-in-class CYP17A/CYP11B2 dual inhibitor. It is an investigational drug for which Laekna obtained the global exclusive licenses from Novartis.It is a next-generation androgen synthesis inhibitor.  

It is a novel, potent, non-steroidal, reversible dual inhibitor of CYP17 and CYP11B2 (aldosterone synthase) that blocks both androgen and aldosterone synthesis. It will be used as a treatment option for metastatic prostate cancer.

Compared to Abiraterone acetate, a CYP17 enzyme inhibitor that causes hyperaldosteronism, which requires long-term use of corticosteroids and may cause serious side effects, LAE001 has demonstrated similar therapeutic efficacy but improved safety profile in patients with drug-resistant mCRPC. Due to its dual inhibition of both CYP17 and CYP11B2, two critical enzymes for testosterone and aldosterone synthesis, LAE001 does not increase aldosterone level, therefore reducing the risk of cardiovascular toxicity and hepatotoxicity related to long-term prednisone use.

Afuresertib (LAE002) is a Class 1 new drug candidate in clinical development, for which Laekna obtained the global exclusive licenses from Novartis. It is a potent next-generation small molecule pan-AKT kinase inhibitor.

Afuresertib (LAE002) is a differentiated oral, small molecule pan-AKT kinase inhibitor that has been investigated in over 10 Phase 1/2 clinical trials, including ovarian cancer, gastric cancer, multiple myeloma, and melanoma. These studies have demonstrated that afuresertib has strong anti-cancer activities and a tolerable safety profile. The global randomized, open-label, multi-center Phase 2 PROFECTA-II clinical trial of afuresertib is the world’s first registration-directed clinical study of a pan-AKT kinase inhibitor to treat platinum-resistant ovarian cancer.

In recent years, AKT (a serine/threonine-protein kinase) has emerged as an important mechanism in oncology, as it plays an important role in regulating various cell functions such as metabolism, survival, proliferation, tissue invasion, and chemotherapy resistance. PTEN deletion and AKT/PIK3CA alteration may lead to excessive activation of the AKT signaling pathways, which is one of the key drivers for cancer growth. The increased activation of the AKT signaling pathway is particularly common in recurrent ovarian cancer, breast cancer, and prostate cancer.