The BeOne Pipeline

Zanubrutinib is a next-generation, highly selective Bruton tyrosine kinase (BTK) inhibitor engineered to deliver near complete and sustained BTK occupancy while minimizing off-target effects. This enhanced selectivity translates into a more favorable safety profile, particularly with respect to cardiac toxicities such as atrial fibrillation. By achieving higher and more consistent therapeutic exposures, zanubrutinib ensures more complete and continuous suppression of B-cell receptor (BCR) signaling, which is critical for the survival and proliferation of malignant B-cells in diseases like chronic lymphocytic leukemia and mantle cell lymphoma.

*Approved in at least one major market, such as the USA, EU, China and/or Japan.

Sonrotoclax is an investigational small molecule B-cell lymphoma-2 (BCL2) inhibitor. It belongs to a class of BCL2 homology 3 (BH3) mimetics. Sonrotoclax is a more selective and pharmacologically potent inhibitor of BCL2 than venetoclax. It’s shorter half-life with no drug accumulation can lead to potentially improved convenience for patients.

*Approved in at least one major market, such as the USA, EU, China and/or Japan.

Tislelizumab is a uniquely designed humanized immunoglobulin G4 (IgG4) anti-programmed cell death protein 1 (PD-1) monoclonal antibody with high affinity and binding specificity against PD-1. It is designed to minimize binding to Fc-gamma (Fcγ) receptors on macrophages, helping the body’s immune cells detect and fight tumors.

*Approved in at least one major market, such as the USA, EU, China and/or Japan.

BGB‑16673 is an orally available Bruton tyrosine kinase (BTK) targeting chimeric degradation activation compound (CDAC) designed to promote the degradation, or breakdown, of both wildtype and mutant forms of BTK, including those that commonly result in resistance to BTK inhibitors in patients who experience progressive disease.

Blinatumomab is a BiTE® (bi-specific T-cell engager) immuno-oncology therapy that targets CD19 surface antigens on T-cells. BiTE molecules fight cancer by helping the body’s immune system detect and target malignant cells by engaging T-cells (a type of white blood cell capable of killing other cells perceived as threats) to cancer cells. By bringing T-cells near cancer cells, the T-cells can inject toxins and trigger cancer cell death (apoptosis).

Tarlatamab is a first-in-class targeted immunotherapy engineered by Amgen researchers that binds to both DLL3 on tumor cells and CD3 on T-cells. Tarlatamab causes T-cell activation, release of inflammatory cytokines, and lysis of DLL3-expressing cells.^2,3

DLL3 is a protein that is expressed on the surface of SCLC cells in up to 96% of patients with SCLC, but is minimally expressed on the surface of healthy cells, making it an exciting target. ^4,5

*Tarlatamab is approved in the U.S. by the Food and Drug Administration and commercialized by Amgen.

Zanidatamab⁶ (HER2 Bispecific Antibody) Zanidatamab is an investigational HER2-targeted bispecific, IgG1-like antibody that can simultaneously bind two non-overlapping epitopes of the human epidermal growth factor 2 (HER2) known as biparatopic binding. This unique design and increased binding results in multiple mechanisms of action, including dual HER2 signal blockade, removal of HER2 protein from the cell surface, and immune-mediated cytotoxicity such as complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP) leading to encouraging antitumor activity in patients.

Zanidatamab is being developed by Jazz and BeOne Medicines, Ltd. under license agreements from Zymeworks, who first developed the molecule.

Pamiparib is a selective PARP1/2 inhibitor, targeting the enzyme poly (ADP-ribose) polymerase (PARP), which plays a crucial role in repairing single-strand DNA breaks.

BG-68501 is a highly potent and selective cyclin-dependent kinase (CDK) 2 inhibitor that blocks elevated Cyclin E and CDK2 activity, which is a key resistance mechanism to commonly used CDK4/6 inhibition treatments in HR+/HER2- breast cancer.

BGB-21447 is highly potent and selective BCL2 inhibitor (a drug that selectively stops a protein called B-cell lymphoma-2 (BCL2)). BCL2 proteins are often overexpressed in some cancers including 70% overexpression in HR+ breast cancer. The combination of BGB-21447 with endocrine therapy (ET)± a selective CDK4i is hypothesized to have therapeutic potential for meaningful clinical benefit in patients with HR+/HER2- BC.

BGB-43395 is an innovative molecule designed to inhibit CDK4, which is a cyclin-dependent kinase that drives cancer cell growth. By selectively inhibiting CDK4 while avoiding CDK6, BGB-43395 can potentially slow cancer cell growth while reducing CDK6 associated hematological toxicities. The combination of BGB-43395 with ET can result in meaningful clinical improvements for patients with HR+/HER2- BC, among other tumor types.

BGB-B455 is a bispecific antibody engineered to redirect effector T-cells to tumor cell killing in a CLDN6-dependent manner. Preclinical studies suggest potent antitumor activity, including efficacy in immunologically cold tumors or those with heterogeneous CLDN6 expression. The molecule has been optimized for high CLDN6 specificity over other claudin family members, coupled with silenced Fc effector function to mitigate off-target and immune-related toxicity. These designs establish BGB-B455 as a promising therapeutic candidate, offering a well-balanced efficacy-safety profile for clinical development in CLDN6-expressing tumors.

BG-C9074 targets B7-H4, a transmembrane glycoprotein in the B7 superfamily with limited expression in normal tissue and upregulated in solid tumors including breast, ovarian, and endometrial cancers. BG-C9074 is a B7-H4 targeting ADC composed of high affinity anti-B7-H4 antibody, enzymatically cleavable linker and a potent TOP1 inhibitor payload. It has demonstrated good internalization and strong bystander killing in preclinical models, as well as dose-dependent activity in clinical setting.

BG-75202 is a potential best-in-class inhibitor for KAT6A/B, which are chromosome histone lysine acyltransferases regulating gene transcription through histone acetylation. ​KAT6 inhibition leads to downregulation of multiple gene transcription and oncogenic signaling pathways. KAT6 has been clinically validated in HR+ HER2- BC​. The combination of BG-75202 with endocrine therapy (ET)± a selective CDK4i is hypothesized to have therapeutic potential for meaningful clinical benefit in patients with HR+/HER2- BC.

BG-75098 is a potential first-in-class degrader of cyclin-dependent kinase (CDK) 2 with remarkable selectivity and potency. BG-75098 uniquely eliminates CDK2, which deactivates CDK2-cyclin E/A complex even with high cyclin E level, which is related to drug resistance in multiple tumor types. BG-75098 is being evaluated in breast cancer and other solid tumors.

BGB-B2033 is a bispecific antibody that activates 4-1BB on CD8 T-cells only in the presence of GPC3-expressing tumor cells, enabling targeted immune cytotoxicity. The anti-tumor activity is anticipated to be enhanced with anti-PD-1 inhibitors such as BeOne’s tislelizumab.

BG-C137 targets Fibroblast Growth Factor Receptor 2b (FGFR2b), which plays a critical role in cell growth, tissue repair and tumor development. In cancers such as gastric cancer, esophageal squamous cell carcinoma, ovarian cancer, breast cancer, and lung cancer, FGFR2b becomes aberrantly activated, leading to uncontrolled tumor growth. BG-C137 utilizes a weaker ligand-blocking mechanism to avoid on-target corneal toxicity. Additionally, it is designed to achieve superior efficacy through targeted toxin delivery to tumor cells and exhibits a strong bystander effect, offering advantages over conventional antibody therapies in overcoming tumor heterogeneity.

Kirsten Rat Sarcoma (KRAS) is a signaling protein that regulates cell processes like growth and division. KRAS mutations occur in about 19% of all tumor types and can be a significant contributor to tumor growth.^9,10,11

BGB-53038 is designed to target mutated KRAS or amplified KRAS proteins to inhibit tumor growth. It has shown broad activity against KRAS mutations and amplification in multiple tumor types in preclinical models and may limit toxicity by sparing other RAS proteins.

BG-C477 targets human carcinoembryonic antigen related cell adhesion molecule 5 (CEACAM5, also known as CEA), whose overexpression has been observed in many types of cancers, such as gastrointestinal cancers and non-small cell lung cancer, but has limited presence on normal tissues. CEA can directly participate in the inhibition of anoikis and implantation of cancer cells, and its overexpression contributes to the progression of many epithelial cancers and to immune dysfunctions. BG-C477 is a potent and specific CEA-targeting ADC composed of a humanized anti-CEA monoclonal antibody, a cleavable linker, and a TOP1 inhibitor payload.

BG-C0902 targets Epidermal Growth Factor Receptor (EGFR) and cellular-Mesenchymal Epithelial Transition (cMET) – two well established oncogenic drivers frequently overexpressed and dysregulated in lung cancers and other solid tumors. BG-C0902 has a differentiated biparatopic design for cMET potentially enabling enhanced inhibition of MET signaling. BG-C0902 has dual targeting EGFR and MET with ADC modality and may offer durable response and broad coverage.

BG-T187 is an antibody engineered to target Epidermal Growth Factor Receptor (EGFR) and cellular-Mesenchymal Epithelial Transition (cMET) – two well established oncogenic drivers frequently overexpressed and dysregulated in lung cancers and other solid tumors. BG-T187 has a differentiated biparatopic design for cMET potentially enabling enhanced inhibition of MET signaling.

BGB-58067 is designed to inhibit the activity of the enzyme Protein Arginine Methyltransferase 5 (PRMT5), which plays a critical role in the survival of cancer cells. These tumors often lack the gene Methylthioadenosine Phosphorylase (MTAP), which normally regulates key metabolic processes. In the absence of MTAP, cancer cells become highly dependent on PRMT5 for growth and survival. In contrast, normal cells retain MTAP function and are less reliant on PRMT5. This difference allows BGB-58067 to targets and selectively kill cancer cells while sparing healthy tissue. BGB-58067 has potential best-in-class characteristics including superior potency, better selectivity, and brain penetration. Preclinical models demonstrated strong synergy between PRMT5i and MAT2Ai.

BG-89894 is a novel Methionine Adenosyltransferase 2A (MAT2A) inhibitor being evaluated for the treatment of solid tumors. BG-89894 targets solid tumors with a genetic deletion of Methylthioadenosine Phosphorylase (MTAP), which is estimated to be present in approximately 15% of all cancer types with the most common including glioblastoma, pancreatic cancer and non-small cell lung cancer. Preclinical data demonstrated superior potency and sustained tumor PD and potential brain penetration property.

BG-60366 is a Chimeric Degradation Activation Compound (CDAC), a type of degrader, that targets Epidermal Growth Factor Receptor (EGFR), a protein that helps cancer cells grow and spread. Some cancers have too much EGFR, making them more aggressive. Unlike traditional drugs that block EGFR, a degrader completely eliminates it, which may be more effective in stopping cancer and overcoming drug resistance. It has broad coverage of EGFR mutations, highly potent across osimertinib-sensitive and resistant EGFR mutations. Meanwhile, it spares wild-type EGFR which is believed to be translated to a better safety profile in clinic.

HPK1 is a key negative feedback regulator of T-cell receptor signaling, which is believed to play a key role in antitumor immune response. In preclinical studies, the inhibition of HPK1 enhanced T-cell activation, which is expected to enhance the anti-tumor activity of anti-PD-1 inhibitors such as BeOne’s tislelizumab.

Xaluritamig is a novel immunotherapy that targets the six-transmembrane epithelial antigen of the prostate 1 (STEAP1), a protein found at high levels in metastatic castration-resistant prostate cancer (mCRPC) cells, and CD3 on T-cells, redirecting the T-cells to specifically recognize and kill the STEAP1-expressing cancer cells.

BGB-45035 is a first-in-class, highly potent, and selective degrader of Interleukin-1 Receptor-Associated Kinase 4 (IRAK4), a key driver of autoimmune and inflammatory diseases through the IL-1R/TLR pathway. BGB-45035 uniquely eliminates IRAK4 entirely – disabling both its kinase activity and scaffold function, offering broad suppression of disease-driving inflammation. BGB-45035 is being evaluated in multiple autoimmune disorders.