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.

In addition to acute plasm membrane repair function, MG53 is found to mitigate inflammation associated with chronic injuries. MG53 has shown effectiveness in cellular repair for injuries of multiple organs (brain, heart, lung, kidney, liver, eye, etc.) based on animal experiments (with mouse, pig, monkey, etc.).

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.

Over the last two years, we have increased scale and yield of manufacturing of Mg53 with purity over 99%. We plan to finish preclinical studies and to be ready for IND submissions to China and US FDA within two years. Please view for a brief introduction.


Highlight Publication:

  1. Membrane-delimited signaling and cytosolic action of MG53 preserve hepatocyte integrity during drug-induced liver injury J Hepatol. 2022 Mar Link
  2. MG53 suppresses NF-κB activation to mitigate age-related heart failure JCI Insight 2021 Sep Link
  3. MG53 Preserves Neuromuscular Junction Integrity and Alleviates ALS Disease Progression. Antioxidants (Basel). 2021 Sep 25 Link
  4. Recombinant MG53 Protein Protects Mice from Lethal Influenza Virus Infection. Am J Respir Crit Care Med 2021 Jan Link
  5. Muscle multiorgan crosstalk with MG53 as a myokine for tissue repair and regeneration. Curr Opin Pharmacol. 2021 Aug Link
  6. MG53, A Tissue Repair Protein with Broad Applications in Regenerative Medicine. Cells 2021 Jan Link
  7. MG53-mediated cell membrane repair protects against acute kidney injury. Sci Transl Med. 2015 Mar LinkComment 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

  8. Treatment of acute lung injury by targeting ​MG53-mediated cell membrane repair. (2014) Nature Communication Link
  9. Recombinant MG53 Protein Modulates Therapeutic Cell Membrane Repair in Treatment of Muscular Dystrophy. (2012) Science Translational Medicine.   LinkComment in: “A Molecular Bandage for Diseased Muscle” Sci Transl Med. Link
  10. MG53 nucleates assembly of cell membrane repair machinery. (2009) Nature Cell Biology.  LinkComment in: “Membrane repair redux: redox of MG53”  Nat Cell Biol Link

    Comment in: “A Molecular Bandage for Diseased Muscle” Sci Transl Med. 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-M8 has completed preclinical studies, submitted IND to China’s FDA Equivalent (CDE), and received class 1 innovative drug candidate designation and approval to start Phase I clinical trial with late-stage cancer patients for various cancers on March 1, 2022.

We’ll prepare IND filing materials with US FDA and target to be ready for US IND filing before end of 2023.

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