CD47 binds SIRPα on the surface of macrophages, and transmits a "do not eat" signal that protects cells from macrophage attack. Newly emerging evidence indicates that this negative signal is used by cancer stem cells to protect themselves from marcophage-mediated destruction. SIRPαFc is an antagonist of the CD47- SIRPα interaction, and is designed to alleviate CD47-mediated suppression and promote anti-tumour responses. It is being developed as a treatment for AML.

CD200-specific monoclonal antibody

Tumour cells exploit the suppressive properties of CD200 to escape attack from the immune system. A CD200 antibody is being developed to alleviate this suppression and thus augment anti-cancer immune responses. A lead CD200 clinical development candidate has been identified and the program is ready to enter formal IND-enabling studies.


Tigecycline is an antibiotic used in hospitals to treat a variety of serious infections. Researchers in Toronto recently discovered that this molecule has strong activity in acute myeloid leukemia (AML): it kills AML tumor cells and leukemic stem cells by a unique mechanism of action. It is currently being evaluated in a multi-centre, phase I study in patients with relapsed or refractory AML.


TTI-1612 is a recombinant soluble form of heparin-binding epidermal growth factor- like growth factor (HB-EGF). It is being developed as a treatment for interstitial cystitis (IC), a chronic bladder disease characterized by low urinary HB-EGF levels and a dysfunctional, "leaky" bladder epithelium. TTI-1612 stimulates the proliferation of bladder epithelial cells and reduces their permeability. Unlike the current IC therapeutics, which are largely palliative in nature, TTI-1612 is designed to target the root cause of IC – dysfunction of the bladder urothelium caused by low levels of HB-EGF. This program has completed phase I testing in IC patients.

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