TRIM-edicine is dedicated to the discovery and development of novel protein therapeutics for the treatment of unmet medical needs. Our technology platforms include:


  • Protein Therapeutics for tissue repair in chronic disease or traumatic injury
  • Biologics for regenerative medicine for genetic disorders involving compromised cellular plasticity and repair capacity
  • Bioactive peptides for pharmaceutical and cosmeceutical applications


The company is built around a core of protein therapeutic approaches that involve novel proteins with remarkable biological properties. These unique proteins target a variety of cellular pathways that are altered in numerous disease states. Currently, TRIM-edicine is developing the following proteins:


  • MG53 – targeting diseases involving chronic and acute tissue damage
  • MG29 – targeting diseases related to aging
  • ATAP  – targeting cancer

Mitsugumin53 (MG53)

Mitsugumin53 (MG53) — MG53, belonging to the TRIM family of proteins, is the first known essential molecular component in the intrinsic cellular membrane repair process. Following instances of membrane damage, the entry of the oxidative extracellular environment results in MG53 oligomerization and translocation of MG53-containing vesicle to the injury site to initiate membrane repair. Muscle fibers lacking in MG53 display defective membrane permeability and increased susceptibility to disease, suggesting that MG53 is a critical component of the membrane repair process. MG53 is endogenous to cardiac and skeletal muscle, thus providing a unique target for therapeutic interventions in systemic diseases such as heart failure, muscular dystrophy, stress-associated muscle injury, and age-related muscle atrophy. Through either the administration of recombinant MG53 protein or pharmacological modulation of endogenous MG53, TRIM-edicine believes it possesses a potentially important therapeutic agent/opportunity targeting several attractive markets.


Highlight Publication:

1. Dual function of MG53 in membrane repair and insulin signaling. (2016) BMB Rep Link

2. Modulation of wound healing and scar formation by MG53 protein-mediated cell membrane repair. (2015) J Biol Chem Link

3. Genome-wide CRISPR screen in a mouse model of tumor growth and metastasis. (2015) Cell Link

“Independent study from Dr. Feng Zhang’s group shows evident that MG53 may play a role in tumor suppression”

4. Cardioprotection of recombinant human MG53 protein in a porcine model of ischemia and reperfusion injury. (2015)  J Mol Cell Cardiol. Link

Comment in: “Mitsugumin-53: Potential biomarker and therapeutic for myocardial ischemic injury?”  (2015) J Mol Cell Cardiol. Link PDF

5. MG53-mediated cell membrane repair protects against acute kidney injury. Sci Transl Med. 2015 Mar Link

Comment in 1: “TRIM family protein protects the kidney” Nature New Drug Discovery Link

Comment in 2: “Mitsugumin 53 mediates repair of the damaged proximal tubular epithelium” Nature Review Nephrology Link PDF

6. Treatment of acute lung injury by targeting ​MG53-mediated cell membrane repair. (2014) Nature Communication Link

7. Recombinant MG53 Protein Modulates Therapeutic Cell Membrane Repair in Treatment of Muscular Dystrophy. (2012) Science Translational Medicine.   Link

Comment in: “A Molecular Bandage for Diseased Muscle” Sci Transl Med. Link

8. MG53 nucleates assembly of cell membrane repair machinery. (2009) Nature Cell Biology.  Link

Comment in: “Membrane repair redux: redox of MG53”  Nat Cell Biol Link





Mitsugumin29 (MG29)

MG29 is a skeletal muscle-specific protein related to the synaptophysin family of proteins and is suggested to be important for normal muscle function. MG29 knockout mice show fragmented sarcoplasmic reticulum (SR), Transverse-Tubule swelling, uncoupled Ca2+ sparks during stress, and greater susceptibility to fatigue, phenotypes which also emerge in aging wildtype muscle. The similarities between MG29 knockout and wildtype aged muscle suggests that downregulated MG29 expression is linked to muscle aging. Through either the administration of recombinant MG29 protein or pharmacological modulation of endogenous MG29, TRIM-edicine believes it possesses a potentially important therapeutic agent/opportunity to target disorders related to aging.


Highlight Publication:

1. Dysfunction of store-operated calcium channel in muscle cells lacking mg29. (2002) Nature Cell Biology.  Link

2.Muscle aging is associated with compromised Ca2+ spark signaling and segregated intracellular Ca2+ release. (2006)  J Cell Biol.  Link




ATAP is a tail-anchoring peptide of the Bcl-2 family of proteins. ATAP is a potent stimulator of apoptosis by inducing changes in mitochondria membrane potential, leading to apoptosis of the cell. TRIM-edicine believes that ATAP represents a potentially important therapeutic agent that targets cancer cells.


Highlight Publication:

1. The tail-anchoring domain of Bfl1 and HCCS1 targets mitochondrial membrane permeability to induce apoptosis. (2007)  J Cell Sci.  Link

2. Amphipathic tail-anchoring peptide and Bcl-2 homology domain-3 (BH3) peptides from Bcl-2 family proteins induce apoptosis through different mechanisms. (2011)  J Biol Chem.  Link

3. Core-shell nanoparticle-based peptide therapeutics and combined hyperthermia for enhanced cancer cell apoptosis. (2014)  ACS Nano.  Link

4. Amphipathic tail-anchoring peptide is a promising therapeutic agent for prostate cancer treatment. (2014)  Oncotarget.  Link