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REFERENCES: J. Biol. Chem. 2011, 286, 4902-4911., J. Biol. Chem. 2007, 282, 21477-21486., J. Am. Chem. Soc. 2006, 128, 14691-14696.!Technology originated in the laboratory of Dr. Vern Schramm at the Albert Einstein College of Medicine!

steve@nanometicslab.com www.nanometicslab.com 646.801.3872

National Institute of Health (NIH) funded laboratory focused on hematology and oncology. Funded by over $3.3 million in SBIR funding since 2010:

•  National Heart Lung and Blood Institute– sickle cell disease •  National Cancer Institute– skin cancer prevention •  National Cancer Institute– triple negative breast cancer

Key Advantages

Pharmacology: Potent efficacy against six different cancers as low as 5 mg/kg.

Toxicity: No toxicity at doses up to 400 mg/kg.

Dosing: Once-daily oral or i.p. dosing suppresses tumor growth in six different mouse xenografts of human cancer.

CMC: Low molecular weight, water soluble salt, with kilogram scale manufacturing underway.

Patent Status: Comprehensive IP por t fo l io inc ludes compos i t ion , preparation and methods of use.

Track Record of Success: Developed in the laboratory of Dr. Vern Schramm at the Albert Einstein College of Medicine, with similar compounds developed for other indications having recently completed Phase II clinical trials.

Community Support: Funded by a $100,000 Avon Foundation Award and a pending $225,000 NIH award.

Development Status: IND-enabling GLP sa fe ty pharmaco logy and toxicology underway.

d71

Days after tumor cell injection

MTDIA Suppresses Tumor Growth and Causes Tumor Regression in Human TNBC Tumors!

(A) Treatment of MDA-MB-468 mouse xenografts with MTDIA caused significant tumor growth suppression. Tumors were grown for 35 days before treatment with oral or i.p. MTDIA. At day 71, the untreated (control) group was treated with MTDIA (i.p.). (B) Selected animals from the ‘Untreated, then treated’ group (1) showed tumor lysis, while cessation of treatment allowed slow regrowth in some mice (2). In others, tumor eradication was complete (3).

•  MTDIA is a picomolar transition state inhibitor of 5’-methylthioadenosine phosphorylase (MTAP).!•  MTDIA administration causes systemic inhibition of MTAP, resulting in whole-body accumulation of

methylthioadenosine (MTA), whole-body decreases in S-adenosyl methionine (Ado MET) levels, and anti-cancer effects.!

MTDIA: A Targeted Oral Therapeutic For Triple Negative Breast Cancer

Ki* = 86 pMMTDIAH

NMeS

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Nanometics is seeking a partner for clinical studies

A

B