Savolitinib is an investigational inhibitor of the mesenchymal epithelial transition factor, or MET, receptor tyrosine kinase, an enzyme which has been shown to function abnormally in many types of solid tumors. We designed savolitinib through chemical structure modification to specifically address kidney toxicity, the primary issue that halted development of several other selective MET inhibitors.

We are currently investigating savolitinib in global partnership with AstraZeneca, both as a monotherapy and in combination with immunotherapy and targeted therapy.

Savolitinib has been approved and marketed in China under the brand name ORPATHYS^®. Savolitinib is not approved for use outside of China.

Surufatinib is a novel small molecule that inhibits the tyrosine kinase activity associated with vascular endothelial growth factor receptor (VEGFR) and fibroblast growth factor receptor (FGFR), which both promote angiogenesis, and colony stimulating factor-1 receptor (CSF-1R), which regulates tumor-associated macrophages.

Surufatinib has been approved and marketed in China under the brand name SULANDA^®. Surufatinib is not approved for use outside of China.

We currently retain all rights to surufatinib worldwide.

The investigational drug candidate sovleplenib is a novel, selective, oral inhibitor of the spleen tyrosine kinase (Syk).

Syk is a major component in B-cell receptor signaling and is an established therapeutic target in multiple subtypes of B-cell lymphomas. Because B-cell malignancies are heterogeneous and patients commonly experience relapse despite current therapies, there is a need for new therapies. Syk is upstream of both BTK and PI3K.

HMPL-523 is being investigated in various hematological cancers such as indolent non-Hodgkin's lymphomas and certain chronic immune diseases in the U.S., Europe, China and Australia.

We currently retain all rights to HMPL-523 worldwide.

Tazemetostat is a methyltransferase inhibitor of EZH2 developed by Epizyme, Inc.  EZH2 catalyzes the methylation of histone H3 which controls expression of various genes and in turn plays a role in the normal physiology of many cell types. Dysregulation of EZH2 has been seen in a wide range of cancers and is associated with poor clinical prognosis and outcomes.

We have a strategic collaboration with Epizyme (a wholly owned subsidiary of Ipsen) to research, develop, manufacture and commercialize tazemetostat in Greater China.  We are exploring the treatment potential of tazemetostat in investigational clinical trials in other solid tumors and hematological malignancies, as a monotherapy and combination therapy in both relapsed and front-line disease settings.

Tazemetostat is approved in the US under the brand name TAZVERIK^®. Tazemetostat is not approved for use outside of the U.S. and Japan.

HMPL-453 is an investigational novel selective small molecule inhibitor that targets fibroblast growth factor receptor (FGFR) 1/2/3, a sub-family of receptor tyrosine kinases. Aberrant FGFR signaling has been found to be a driving force in tumor growth (through tissue growth and repair), promotion of angiogenesis and resistance to anti-tumor therapies.  Abnormal FGFR gene alterations are believed to be the drivers of tumor cell proliferation in several solid tumor settings.

We currently retain all rights to HMPL-453 worldwide.

The investigational drug candidate amdizalisib is a novel, selective small molecule inhibitor targeting the isoform phosphoinositide 3’-kinase delta (PI3Kδ), a key component in the B-cell receptor signaling pathway. We have designed amdizalisib  with increased PI3Kδ isoform selectivity. Amdizalisib ’s pharmacokinetic properties have been found to be favorable with good oral absorption, moderate tissue distribution and low clearance in pre-clinical pharmacokinetic studies.

Amdizalisib is being investigated in studies in the U.S., Europe, China and Australia in various subtypes of advanced relapsed or refractory non-Hodgkin's lymphoma, including follicular lymphoma and marginal zone lymphoma.

We currently retain all rights to amdizalisib  worldwide.

HMPL-306 is an investigational novel selective small molecule dual inhibitor of isocitrate dehydrogenase (IDH) 1 and 2 mutations. IDH1 and IDH2 mutations have been implicated as drivers of certain hematological malignancies, gliomas and solid tumors, particularly among acute myeloid leukemia patients. Cytoplasmic mutant IDH1 and mitochondrial mutant IDH2 have been known to switch to the other form when targeted by an inhibitor of IDH1 mutant alone or IDH2 mutant alone. Cancer patients harboring either IDH mutation have been known to develop resistance to therapies that target IDH1 or IDH2 through isoform switching.

We currently retain all rights to HMPL-306 worldwide.

HMPL-760 is a novel third-generation BTK inhibitor and our eleventh in-house discovered small molecule investigational oncology drug candidate. It is a reversible, non-covalent inhibitor of BTK wild type and BTK C481S mutant enzymes. C481S is a key resistance mechanism for first-generation BTK inhibitors.

We currently retain all rights to HMPL-760 worldwide.

HMPL-295 is a novel investigational inhibitor of ERK. ERK is a downstream component of the RAS-RAF-MEK-ERK signaling cascade (MAPK pathway). This is our first of multiple candidates in discovery targeting the MAPK pathway.

RAS-MAPK pathway is dysregulated in human diseases, particularly cancer, in which mutations or non-genetic events hyper-activate the pathway in more than 50% of cancers. Activating mutations in RAS genes occur in more than 30% of cancers. RAS and RAF predict worse clinical prognosis in a wide variety of tumor types, mediate resistance to targeted therapies, and decrease the response to the approved standards of care. In the MAPK pathway, KRAS inhibitors are under clinical evaluation, and acquired resistance develops for RAF/MEK targeted therapies. ERK inhibition has the potential to overcome or avoid the intrinsic or acquired resistance from upstream mechanisms such as these.

We currently retain all rights to HMPL-295 worldwide.

HMPL-653 is an investigational novel,  selective inhibitor of CSF-1R designed to target malignant driven tumors as a monotherapy or in combinations.

CSF-1R is usually expressed on the surface of macrophages and can promote growth and differentiation of macrophages after binding with its ligand, CSF-1. A number of in vitro studies have shown that blocking the CSF-1R signaling pathway could modulate the tumor microenvironment, relieve tumor immunosuppression, and synergize with other anti-cancer therapies such as immune checkpoint inhibitors. It has been demonstrated in several clinical studies that other CSF-1R inhibitors could be used to treat tenosynovial giant cell tumor (TGCT), and to treat a variety of malignancies through combination with immuno-oncology and/or other therapeutic agents.

We currently retains all rights to HMPL-653 worldwide.

HMPL-A83 is an investigational novel IgG4-type humanized anti-CD47 monoclonal antibody. CD47 is a cell surface transmembrane protein that is ubiquitously expressed on virtually all human cells. The overexpression of CD47 is reported in a variety of tumors and is believed to be associated with immune escape from macrophage-mediated phagocytosis. HMPL-A83 blocks CD47 binding to Signal regulatory protein (SIRP) α and disrupts the “do not eat me” signal that cancer cells use to shield themselves from the immune system.

We currently retain all rights to HMPL-A83 worldwide.

A significant portion of patients with non-small cell lung cancer go on to develop brain metastasis. Patients with brain metastasis suffer from poor prognosis. Epitinib is a selective oral epidermal growth factor receptor (EGFR) inhibitor. Investigational studies suggest that epitinib may overcome the blood-brain barrier.

We currently retain all rights to epitinib worldwide.