3728 Jinke Rd, Building 1, West Wing, Shanghai, China
info@tyligand.com
R & D Strategy
Our core business model centers on the in-house discovery and development of innovative therapeutics in the field of oncology, particularly small molecule and ADC drug candidates.
We have established proprietary and fully integrated small molecule and ADC innovation platforms, positioning us as a dual-engine innovator.
These capabilities enable the development of highly-differentiated small molecules as well as ADCs featuring novel payloads and high-performance linkers, accelerating the advancement of therapeutics with enhanced efficacy and clinical potential.
Oncology
Driven by environmental changes, increasing average life expectancy, and the successful control of other diseases, cancer has emerged as one of the leading causes of mortality worldwide. Globally, there are nearly 20 million new cancer cases and approximately 10 million cancer-related deaths annually. The cumulative risk of developing cancer before the age of 75 is 21%, and the risk of dying from it is 18%. In China, malignant tumors account for one-quarter of all deaths. Approximately 10,000 individuals are diagnosed with cancer every day, and the 5-year relative survival rate is merely 40%.
The etiology of cancer is highly complex, yet universally characterized by uncontrolled cellular proliferation within the body. To maintain normal physiological functions, the processes of cell growth, maturation, proliferation, and apoptosis in various tissues are governed by strict regulatory mechanisms. Oncogenesis initiates when this orderly process collapses, leading to abnormal cellular differentiation and unrestrained proliferation. These malignant cells can evade immune surveillance and destruction, infiltrate surrounding tissues, and induce angiogenesis—the formation of new blood vessels—to secure the oxygen and nutrients required for their continuous growth. Ultimately, they can metastasize to other organs via the circulatory or lymphatic systems, forming secondary tumors distant from the primary lesion.
The genetic alterations that cause cancer generally fall into three main categories: mutations in proto-oncogenes, inactivation of tumor suppressor genes, and deficiencies in DNA repair genes. These alterations are commonly referred to as cancer "driver genes." Proto-oncogenes are inherently involved in normal cell growth and division; however, when altered to become hyperactive, they can transform into oncogenes, driving uncontrolled cellular proliferation and survival. Tumor suppressor genes normally function to regulate cell growth and division; when they are mutated, inactivated, or have their expression suppressed, malignant cells divide and proliferate uncontrollably. DNA repair genes are responsible for correcting damaged DNA; when these genes become deficient, genetic errors are passed on to subsequent cell generations, potentially leading to oncogenesis.
We focus on the underlying oncogenic mechanisms at the molecular level and the characteristics of tumor tissues. We are committed to discovering drugs capable of precisely modulating oncogenes and their downstream protein signaling pathways, thereby providing effective, safe, convenient, and accessible therapeutic options for patients worldwide.