On September 30, 2019 Medicenna Therapeutics Corp. ("Medicenna" or "the Company") (TSX: MDNA,OTCQB: MDNAF), a clinical stage immunotherapy company developing first-in-class Superkines and Empowered Cytokines, reported the presentation of new pre-clinical data from its IL-2 Superkine program (Press release, Medicenna Therapeutics, SEP 30, 2019, View Source [SID1234539962]). The data was presented as a poster entitled "Long-acting MDNA109: Emerging IL-2 Superkines displaying potent anti-tumoral responses" this past weekend on September 27th, 2019 at the International Cancer Immunotherapy Conference (CIMT) (Free CIMT Whitepaper) held in Paris, France.

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The presentation by Dr. Minh To, Director of Pre-clinical Development at Medicenna, reported additional preclinical data to support the differentiating characteristics of long-acting MDNA109 variants and their potency in vitro and in vivo from other long-acting IL2 programs.

"In preclinical studies, we have combined MDNA109 variants with checkpoint inhibitors and we see very dramatic cure rates in mice," states Dr. Minh To. "In addition, when you re-challenge these mice on the opposite flank with more tumor, these tumors simply don’t grow, showing long-term protection against tumor development and prevention of relapse."

"We have an exciting pre-clinical program being built around the IL-2 Superkine platform, where we just announced our lead clinical candidate, MDNA19," states Rosemina Merchant, Chief Development Officer of Medicenna. "By engineering a potent CD122 directed Superkine with a superior safety and PK profile, we believe that MDNA19 could emerge as a best-in-class IL-2 with its unique ability to preferentially stimulate cancer killing T cells as reported by an independent study published last month in Nature Communications."

Highlights from the presentation are summarized below:

High potency towards naïve effector T cells but diminished potency on unwanted regulatory T cells (Tregs). Of the long-acting MDNA109 variants, MDNA19 is superior in having decreased binding to CD25 and increased affinity to CD122, therefore selectively activating cancer killing CD8 T cells instead of tumor protecting Tregs.

Potent effects as monotherapy with improved PK characteristics. In CT26 (mouse colon cancer) and B16F10 (mouse melanoma) models, treatment with long acting variants of MDNA109 (bi-weekly for 2 weeks or once weekly for 2 or 3 weeks) potently inhibited tumor growth. These data suggest that long-acting MDN109 variants could lead to potent therapeutic effects with a dosing schedule similar to that used for immune checkpoint inhibitors (CPI). In addition, the results also confirm that different protein scaffolds may be used to extend the half life of MDNA109 and can provide similar tumor control as MDNA19.

Compelling preclinical synergism with immune checkpoint inhibition: In a pre-established colon cancer CT26 model, long-acting MDNA109 variants co-administered with the immune-checkpoint blocker anti-cytotoxic T-Lymphocyte-Associated Protein (CTLA)4, showed significant tumor growth inhibition with as many as 89% of animals remaining tumor-free for over 175 days.

Strong Memory Response. Furthermore, tumor free animals receiving a second and third re-challenge of the tumor without further treatment remained tumor free in up to 100% of mice, demonstrating development of a strong memory response with the ability to prevent tumor relapses.
About MDNA109

Developed by scientists at Stanford University, MDNA109 is an engineered version of IL-2 that binds up to 200 times more effectively to IL-2Rβ (CD122), thus greatly increasing its ability to activate and proliferate the immune cells needed to fight cancer. MDNA109 is an IL-2 Superkine that preferentially drives the expansion and responses of effector T cells and Natural Killer (NK) cells over Treg cells. It is the only IL-2 in development with a distinct mechanism by virtue of its high affinity towards CD122 allowing it to effectively combat NK cell anergy (exhaustion) which occurs frequently after cancer immunotherapy. MDNA19 is a long-acting version of MDNA109 with diminished binding to Tregs.