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
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.