The innovative research and development efforts of LoxiGen are currently concentrated on treatment of resistant-refractory TNBC patients who do not benefit currently available therapeutics in the market. At LoxiGen, we focus on addressing the overlooked need to identify novel and effective treatment strategies that will improve the benefit of the standard-of-care chemotherapy in TNBC patients who are succumbed to low rates of survival. Overexpression of lysyl oxidase family proteins have been previously associated with ECM stiffness and gain of aggressive traits, such as chemoresistance and metastasis¹. Inhibiting LOX, the founding member of the family in highly stiff desmoplastic tumors, including breast and pancreatic tumors, impairs ECM crosslinking, reduces tumor stiffness and increases the efficacy of chemotherapy through various mechanisms, e.g., increased drug penetration^2,3. In addition, LOX that is secreted from the hypoxic breast tumor cells accumulates at premetastatic sites, crosslinking collagen and is involved in pre-metastatic niche formation⁴. Inhibiting LOX blocks metastatic growth, supporting the therapeutic potential of targeting LOX to treat metastatic disease^2,4. A scheme of the therapeutic potential of targeting LOX to overcome chemoresistance and block metastatic growth in is provided below.