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Recent News
01 March 2024
News
We are excited to announce a strategic collaboration between Enamine, the world's leading provider of chemical building blocks, compound libraries, and biology services, and Genez International, a prominent enterprise with 15 years of experience in cross-border supply management, biopharmaceutical research and development, semiconductor equipment, and high-definition digital imaging systems.
21 February 2024
Press Release
Cresset recently announced a collaboration with Enamine, the world’s leading provider of chemical building blocks and drug discovery services to develop innovative new solutions for the early drug discovery process.
11 January 2024
Press Release
SyntheticGestalt, a research and development company specializing in the application of AI to the life sciences domain, and Enamine, the world’s leading provider of chemical building blocks, screening compounds, and integrated drug discovery services, have announced the start of a joint effort to create a suite of AI models that will enable the generation of synthetically accessible biologically active compounds with optimized physicochemical and ADME/ Tox properties. The models will be applicable to the compound discovery initiatives of SyntheticGestalt, as well as its service for both academic users and pharmaceutical companies.
Cells
2020, 9 (10), 2272
DOI:
10.3390/cells9102272
Adams V.; Gussen V.; Zozulya S.; Cruz A.; Moriscot A.; Linke A.; Labeit S.
Patients with malignant tumors frequently suffer during disease progression from a syndrome referred to as cancer cachexia (CaCax): CaCax includes skeletal muscle atrophy and weakness, loss of bodyweight, and fat tissues. Currently, there are no FDA (Food and Drug Administration) approved treatments available for CaCax. Here, we studied skeletal muscle atrophy and dysfunction in a murine CaCax model by injecting B16F10 melanoma cells into mouse thighs and followed mice during melanoma outgrowth. Skeletal muscles developed progressive weakness as detected by wire hang tests (WHTs) during days 13–23. Individual muscles analyzed at day 24 had atrophy, mitochondrial dysfunction, augmented metabolic reactive oxygen species (ROS) stress, and a catabolically activated ubiquitin proteasome system (UPS), including upregulated MuRF1. Accordingly, we tested as an experimental intervention of recently identified small molecules, Myomed-205 and -946, that inhibit MuRF1 activity and MuRF1/MuRF2 expression. Results indicate that MuRF1 inhibitor fed attenuated induction of MuRF1 in tumor stressed muscles. In addition, the compounds augmented muscle performance in WHTs and attenuated muscle weight loss. Myomed-205 and -946 also rescued citrate synthase and complex-1 activities in tumor-stressed muscles, possibly suggesting that mitochondrial-metabolic and muscle wasting effects in this CaCax model are mechanistically connected. Inhibition of MuRF1 during tumor cachexia may represent a suitable strategy to attenuate skeletal muscle atrophy and dysfunction.