QLSF Biotherapeutics has leveraged multi-format bispecific platforms to optimally elicit potent anti-tumor immunity while sparing normal tissues.

Our pipeline encompasses a wide range of therapeutic modalities for diverse oncological indications.

 Checkpoint Blockade

T Cell Redirection

Phagocytosis Enhancement






Phase I

QL415 Tumor Targeted Cytokine

QL301 PD-L1 x 4-1BB Bispecific Antibody

A bispecific antibody targeting PD-L1-positive tumors stimulates T cell via 4-1BB

QL301 activates 4-1BB only when concurrently engaged to PD-L1, an immune checkpoint mediator elevated in the immuno-suppressive tumor microenvironment. Unwanted toxicity associated with non-specific activation of 4-1BB is therefore minimized. QL301 blocks the interaction of PD-1 with PD-L1 independent of 4-1BB binding. The combination of 4-1BB activation and PD-L1 blockade promotes a robust and lasting anti-tumor immune response. Preliminary data indicates that QL301 is safe in rhesus monkeys. Non-human primate toxicology study is expected to be completed by Q3 2020. IND filling is expected by Q2 2021.

High Avidity Binding

Minimal Binding

QL401 Tumor Targeted CD47 Blocker

Selective CD47 targeting to improve therapeutic windows

The ubiquitous expression of CD47 on normal cells, including red blood cells, presents a therapeutic challenge. Systemic targeting of CD47, by either anti-CD47 monoclonal antibodies or SIRPα-Fc fusion proteins, yields only moderate clinical benefit due to severe adverse side effects, mainly anemia. QLSF has developed tumor targeted CD47 bispecific antibodies with reduced binding to red blood cells while retaining potent phagocytic activation of macrophages in vitro and delayed tumor growth in vivo. Our lead candidate is well produced with drug-like properties.

QL315 LRRC15 x CD3 Bispecific T Cell Engager

A bispecific T cell engager targeting both tumor and stromal cells

Simultaneous binding of a T cell bispecific antibody to CD3 on T cell and a tumor cell surface antigen results in the formation of an immune synapse, which leads to activation and proliferation of the T cell and subsequent killing of the tumor cell. T cell bispecific antibody mediated killing of tumor cell does not require pre-existing immunity and may occur independently of T cell specificity, activation, and differentiation status. This allows for re-activation of immune response in poorly immunogenic “cold” tumors.

Unlike conventional T cell bispecific engager, QL315 is uniquely designed to target both the tumor and its stromal components via binding of LRRC15, an antigen shared by both and highly upregulated in several types of solid tumors. QL315 is optimized for specificity and potency by carefully fine tuning the avidity and affinity of both LRRC15 and CD3 targeting moieties. This ensures maximum efficacy while reducing unwanted toxicity for a wider therapeutic window.

View our poster presented at the 2020 AACR Meeting.