Our Pipeline

We are focused on two target therapeutic areas: oncology and immunological diseases.

We have created a broad pipeline of drug candidates.  We have taken a chemistry-focused approach to develop highly selective small molecule tyrosine kinase inhibitors that are intended to have potentially global best-in-class efficacy and are deliberately engineered to improve drug exposure and reduce known class-related toxicities.

Some of our current drug candidates may have the potential to be global first-in-class therapies, while others may be sufficiently differentiated to potentially be global best-in-class, next generation therapies with a superior profile compared to existing approved drugs that act against the relevant kinase targets.

For more information on recent developments, please refer to our latest presentations or our latest financial reports.

Summary Chart

Updated as of March 13, 2017.
Chi-Med Pipeline August 02, 2016

Notes: * = when an NDA submission is possible based on the receipt of favorable clinical data; Proof-of-concept = Phase Ib/II study (the dashed lines delineate the start and end of Phase Ib); combo = in combination with; brain mets = brain metastasis; VEGFR = vascular endothelial growth factor receptor; TKI = tyrosine kinase inhibitor; EGFR = epidermal growth factor receptor; NET = neuroendocrine tumors; ref = refractory, which means resistant to prior treatment; T790M= EGFR resistance mutation; EGFRm+ = epidermal growth factor receptor activating mutations; EGFR wild-type = epidermal growth factor receptor wild-type; 5ASA = 5-aminosalicyclic acids; chemo = chemotherapy; c-Met+ = c-Met gene amplification; c-Met O/E = c-Met over-expression; MS = Multiple Sclerosis; RA = Rheumatoid Arthritis; Aus = Australia; SK = South Korea; PRC = People’s Republic of China; UK = United Kingdom; US = United States; EU = Europe; Global = more than 1 country.



Savolitinib (AZD6094 / HMPL-504 / volitinib) is a potential global first-in-class inhibitor of the mesenchymal epithelial transition factor, or c-Met, receptor tyrosine kinase, an enzyme which has been shown to function abnormally in many types of solid tumors.  We developed savolitinib as a potent and highly selective oral inhibitor that was designed to address renal toxicity, the primary issue that has prevented other selective c-Met inhibitors from further clinical development.  In Phase I clinical studies, savolitinib has shown promising signs of clinical efficacy, causing tumor size reduction in patients with c-Met gene amplification in papillary renal cell carcinoma, non-small cell lung cancer, colorectal cancer and gastric cancer.

We are currently testing savolitinib in partnership with AstraZeneca in multiple parallel proof-of-concept studies, both as a monotherapy and in combination with other targeted therapies, immunotherapies, and chemotherapy.  In June 2016 we published a detailed summary of all current savolitinib clinical trials covering multiple patient populations, please click here for the summary.



Fruquintinib (HMPL-013) is a highly selective and potent oral inhibitor of the vascular endothelial growth factor receptor, or VEGFR, and consequently we believe it has the potential to be a global best-in-class VEGFR inhibitor for many types of solid tumors. Based on pre-clinical and clinical data to date, fruquintinib’s kinase selectivity has been shown to reduce off-target toxicity, allowing for drug exposure that is able to fully inhibit VEGFR, a protein ligand which contributes to the growth of tumors, and use in potential combinations with other targeted therapies and chemotherapy in earlier lines of treatment with larger patient populations. We believe these are major points of differentiation compared to other small molecule VEGFR inhibitors that have already been approved, such as sunitinib, sorafenib and regorafenib.

In partnership with Eli Lilly, we are currently studying fruquintinib for the treatment of colorectal cancer, non-small cell lung cancer and gastric cancer in China.



Sulfatinib (HMPL-012) is an oral drug candidate that selectively inhibits the tyrosine kinase activity associated with VEGFR and fibroblast growth factor receptor 1, or FGFR1, a receptor for a protein which also plays a role in tumor growth. Our published Phase I clinical data indicate that sulfatinib has the highest objective response rate, or the proportion of patients with tumor shrinkage of more than 30%, reported to date in patients with neuroendocrine tumors. The objective response rate of 35% observed for sulfatinib in this study compares favorably to less than 10% for sunitinib and everolimus, the only two currently approved single agent therapies for neuroendocrine tumors.

Sulfatinib is the first oncology candidate that we have taken through proof-of-concept in China, and expanded to a U.S. clinical study ourselves. We currently retain all rights to sulfatinib worldwide.



Epidermal growth factor receptor, or EGFR, inhibitors have revolutionized the treatment of non-small cell lung cancer with EGFR activating mutations.  However, existing EGFR inhibitors such as gefitinib and erlotinib cannot penetrate the blood-brain barrier effectively, leaving the majority of patients with brain metastasis without an effective therapy.  In contrast, epitinib (HMPL-813) is a potent and highly selective oral EGFR inhibitor designed to optimize brain penetration and has demonstrated brain penetration and efficacy in pre-clinical studies.  If epitinib is able to provide clinical benefit to non-small cell lung cancer patients with brain metastases in its clinical trials in China, we believe that, subject to regulatory approval, we will be well-positioned to address a major global unmet medical need.  We currently retain all rights to epitinib worldwide.



Current EGFR inhibitors on the market are less effective at treating solid tumors with wild-type EGFR activation, which are EGFR proteins without activating mutations. These tumors include head and neck, esophageal and non-small cell lung cancers, for which there are few effective treatments, representing a major unmet medical need. In contrast, theliatinib is a potent and highly selective oral EGFR inhibitor engineered to have significantly greater binding affinity to wild-type EGFR proteins.

As a result, theliatinib (HMPL-309) more effectively inhibits EGFR wild-type activity as compared to existing EGFR targeted therapies and has demonstrated superior anti-tumor activity in our pre-clinical studies among tumors with wild-type EGFR.  We currently retain all rights to theliatinib worldwide.



We believe HMPL-523 is a potential global first-in-class oral inhibitor targeting the spleen tyrosine kinase, or Syk, a key protein involved in B-cell signalling. Modulation of the B-cell signalling system has been proven to significantly advance the treatment of certain chronic immune diseases, such as rheumatoid arthritis. To date, only monoclonal antibody modulators, which seek to use the patient’s own immune system to treat the disease, have been approved. HMPL-523, as an oral drug candidate, may have important advantages over intravenous monoclonal antibody immune modulators in that small molecule compounds clear the system faster, thereby reducing the risk of infections from sustained suppression of the immune system. Moreover, other drug development companies have tried to design small molecule Syk inhibitors for the treatment of chronic immune diseases. However, no drug products targeting Syk have been approved to date due to severe off-target toxicity side effects, such as hypertension, as a result of poor kinase selectivity. HMPL-523 is a potent and highly selective oral inhibitor specifically designed to overcome these off-target toxicity issues.

We believe the market potential for a successful Syk inhibitor is substantial. For example, the estimated size of the global market for rheumatoid arthritis drugs was approximately $34 billion in 2014 and is projected to grow to approximately $45 billion in 2020, according to Frost & Sullivan. We currently retain all rights to HMPL -523 worldwide.



The targeting of PI3Kδ (delta) for B-cell malignancies is gaining an increasingly high profile with idelalisib gaining fast track approval in mid-2014 in multiple hematological cancer indications.  Duvelisib, another high profile PI3Kδ inhibitor, is also in Phase III in various hematological cancer indications.  There is also increasing evidence that PI3Kδ inhibitors are effective in the ibrutinib-resistant mutant population, ibrutinib being an important BTK inhibitor for several types of B-cell malignancies.

We have designed HMPL-689 with superior PI3K isoform selectivity, in particular to spare PI3Kɣ (gamma) to minimize the serious infection observed with duvelisib due to its strong immune suppression.  HMPL-689 potency, particularly at the whole blood level allows for reduced daily doses to minimize compound related toxicity such as the high level of liver toxicity observed with the idelalisib 150mg twice-daily dose regime.  HMPL-689’s pharmacokinetic properties have been found to be favorable with expected good oral absorption, moderate tissue distribution and low clearance, suitable for once daily dosing.  It is also expected that HMPL-689 will have low risk of drug accumulation and drug/drug interaction due to Cytochrome P450 (CYP) inhibition/induction.

Given the above, we believe that HMPL-689 has the potential to be a best-in-class PI3Kδ agent, superior to both idelalisib and duvelisib. We currently retain all rights to HMPL -689 worldwide.



Activation of the Fibroblast growth factor receptor, or FGFR, pathway through the phosphorylation of various downstream molecules ultimately leads to increased cell proliferation, migration and survival. FGF/FGFR signaling regulates a wide range of basic biological processes, including tissue development, angiogenesis, and tissue regeneration. Given the inherent complexity and critical roles in physiological processes, dysfunction in the FGF/FGFR signaling leads to a number of developmental disorders and is consistently found to be a driving force in cancer.

HMPL-453 is a highly selective and potent, small molecule that targets FGFR 1/2/3 with an IC50 in the low nanomolar range. In preclinical studies, HMPL-453 exhibited strong anti-tumor activity that correlated with target inhibition in tumor models with abnormal FGFR activation. It has good pharmacokinetic properties characterized by rapid absorption following oral dosing, good bioavailability, moderate tissue distribution and moderate clearance in all pre-clinical animal species. HMPL-453 was found to have little inhibitory effect on major cytochrome P450 enzymes, indicating low likelihood of drug-to-drug interaction issues.

We currently retain all rights to HMPL -453 worldwide.



HMPL-004 is a proprietary botanical drug for the treatment of inflammatory bowel diseases, namely ulcerative colitis and Crohn’s disease.  As part of our broad gastrointestinal disease research and development joint venture with Nestle Health Science, Nutrition Science Partners Limited, HMPL-004 was in global Phase III registration trials during 2013 and 2014.

In April 2013, NSP initiated the NATRUL-3 global Phase III registration trial in mild-to-moderate ulcerative colitis patients on HMPL-004, in combination treatment with 5-ASAs, and conducted an interim analysis in mid-August 2014. The interim analysis was intended to assess both futility, in terms of efficacy and safety on approximately one-third of the 420 planned patients in NATRUL-3.  The result of the interim analysis was that HMPL-004 showed no overall material effect over the placebo-arm patients and consequently the NATRUL-3 study was terminated and the data un-blinded. Subsequent analysis of the un-blinded NATRUL-3 data showed clear inconsistency with the Phase IIb study in efficacy among patients who had been on 5-ASAs for less than one year prior to NATRUL-3 (49% of the patients).  NSP is in the process of developing a more concentrated version of HMPL-004.