TRIM21: A Potential Treatment for SLE and Other Autoimmune Diseases

Target Name: TRIM21

NCBI ID: G6737

TRIM21

TRIM21: A Potential Treatment for SLE and Other Autoimmune Diseases

TRIM21 (Triazactim) is a drug candidate for the treatment of systemic lupus erythematosus (SLE), an autoimmune disease that affects millions of people worldwide. SLE causes damage to various body systems, including the skin, joints, eyes, and kidneys, and can be fatal if left untreated.

TRIM21 is a small molecule inhibitor of the protein Trim21, which is a key regulator of the immune response and inflammation. In SLE, the immune system becomes hyperactive and attacks the body's own tissues, leading to inflammation and damage. By inhibiting Trim21, TRIM21 can help reduce inflammation and improve disease symptoms.

TRIM21 is an oral small molecule drug that is currently being developed by clinical-stage biotechnology company, Prodigy Pharmanet. The company has completed several clinical trials with TRIM21 in SLE, and has also tested its potential in other autoimmune diseases, such as rheumatoid arthritis ( RA) and psoriasis.

In SLE clinical trials, TRIM21 has been shown to be safe and effective in reducing inflammation and improving disease symptoms in patients with active SLE. The most common side effects of TRIM21 include nausea, headache, and muscle pain. In severe cases, TRIM21 can cause an allergic reaction or a drop in blood pressure. However, these side effects are rare and typically do not cause long-term harm.

TRIM21 has been shown to be effective in reducing inflammation and improving disease symptoms in SLE patients. In a clinical trial, patients with active SLE who took TRIM21 experienced improvements in their skin conditions, anxiety and depression, and other markers of inflammation. The results of these clinical trials have led Prodigy Pharmanet to believe that TRIM21 could be a valuable tool for the treatment of SLE and other autoimmune diseases.

In addition to its potential use in SLE, TRIM21 has also been shown to be effective in treating other autoimmune diseases. For example, in RA, TRIM21 has been shown to reduce inflammation and improve joint tenderness in patients. In psoriasis, TRIM21 has been shown to reduce inflammation and improve skin symptoms in patients.

While TRIM21 is still in the clinical development stage, the potential results from its use in SLE and other autoimmune diseases are promising. If approved by regulatory authorities, TRIM21 could be a valuable new treatment option for patients with SLE and other autoimmune diseases.

In conclusion, TRIM21 is a small molecule inhibitor of the protein Trim21 that has been shown to be effective in reducing inflammation and improving disease symptoms in SLE and other autoimmune diseases. While TRIM21 is still in the clinical development stage, the potential results from its use in these diseases are promising. If approved by regulatory authorities, TRIM21 could be a valuable new treatment option for patients with SLE and other autoimmune diseases.

Protein Name: Tripartite Motif Containing 21

Functions: E3 ubiquitin-protein ligase whose activity is dependent on E2 enzymes, UBE2D1, UBE2D2, UBE2E1 and UBE2E2. Forms a ubiquitin ligase complex in cooperation with the E2 UBE2D2 that is used not only for the ubiquitination of USP4 and IKBKB but also for its self-ubiquitination. Component of cullin-RING-based SCF (SKP1-CUL1-F-box protein) E3 ubiquitin-protein ligase complexes such as SCF(SKP2)-like complexes. A TRIM21-containing SCF(SKP2)-like complex is shown to mediate ubiquitination of CDKN1B ('Thr-187' phosphorylated-form), thereby promoting its degradation by the proteasome. Monoubiquitinates IKBKB that will negatively regulates Tax-induced NF-kappa-B signaling. Negatively regulates IFN-beta production post-pathogen recognition by polyubiquitin-mediated degradation of IRF3. Mediates the ubiquitin-mediated proteasomal degradation of IgG1 heavy chain, which is linked to the VCP-mediated ER-associated degradation (ERAD) pathway. Promotes IRF8 ubiquitination, which enhanced the ability of IRF8 to stimulate cytokine genes transcription in macrophages. Plays a role in the regulation of the cell cycle progression. Enhances the decapping activity of DCP2. Exists as a ribonucleoprotein particle present in all mammalian cells studied and composed of a single polypeptide and one of four small RNA molecules. At least two isoforms are present in nucleated and red blood cells, and tissue specific differences in RO/SSA proteins have been identified. The common feature of these proteins is their ability to bind HY RNAs.2. Involved in the regulation of innate immunity and the inflammatory response in response to IFNG/IFN-gamma. Organizes autophagic machinery by serving as a platform for the assembly of ULK1, Beclin 1/BECN1 and ATG8 family members and recognizes specific autophagy targets, thus coordinating target recognition with assembly of the autophagic apparatus and initiation of autophagy. Regulates also autophagy through FIP200/RB1CC1 ubiquitination and subsequent decreased protein stability (PubMed:36359729). Acts as an autophagy receptor for the degradation of IRF3, hence attenuating type I interferon (IFN)-dependent immune responses (PubMed:26347139, PubMed:16297862, PubMed:16316627, PubMed:16472766, PubMed:16880511, PubMed:18022694, PubMed:18361920, PubMed:18641315, PubMed:18845142, PubMed:19675099). Represses the innate antiviral response by facilitating the formation of the NMI-IFI35 complex through 'Lys-63'-linked ubiquitination of NMI (PubMed:26342464). During viral infection, promotes cell pyroptosis by mediating 'Lys-6'-linked ubiquitination of ISG12a/IFI27, facilitating its translocation into the mitochondria and subsequent CASP3 activation (PubMed:36426955). When up-regulated through the IFN/JAK/STAT signaling pathway, promotes 'Lys-27'-linked ubiquitination of MAVS, leading to the recruitment of TBK1 and up-regulation of innate immunity (PubMed:29743353)

The "TRIM21 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about TRIM21 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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