p62

P62-mediated mitophagy inducer (PMI) is a regulator of mitophagy.

ML162 is a covalent glutathione peroxidase 4 (GPX4) inhibitor that induces ferroptosis. ML162 has antitumor activity and selectively inhibits cell lines expressing mutant RAS oncogenes.

p62-ZZ Ligand-Linker Conjugate 1 is a conjugate of the p62-ZZ domain ligand and linker. This compound is utilized in the synthesis of AUTOTACVinclozolinM2-2204.

p62-ZZ ligand 1 (Compound 7) functions as a p62-ZZ ligand and is utilized in the synthesis of VinclozolinM2-2204.

NMS-P626 functions as an inhibitor targeting TRKA, TRKB, and TRKC, exhibiting IC 50 values of 8 nM, 7 nM, and 3 nM respectively. It effectively suppresses KM12 cell growth by inhibiting the phosphorylation of TPM3-TRKA and the subsequent downstream signaling, demonstrating an IC 50 of 19 nM specifically for KM12 cells. This compound is applicable in the study of colorectal cancer.

RSL3 (RSL3 1S) is an inhibitor of GPX4, and inhibits system xc- that blocks GSH synthesis (IC50=100 nM). RSL3 is a VDAC-independent activator of ferroptosis that is selective for tumor cells carrying oncogenic RAS.

Z-FY-CHO (Z-Phe-Tyr-CHO) is a selective histone L (Cat L) inhibitor that promotes autophagy, reduces the accumulation of P62, and blocks the activation of caspase-3 and PARP.

Compound Fr14273 is a natural product for research related to life sciences. The catalog number is Fr14273 and the CAS number is 551-93-9.

Bifendate (Bifendatatum) is commonly used to treat the transaminase elevation that caused by viral hepatitis and drug-induced liver injury.

ARP 101 is an effective selective matrix metalloproteinase-2 (MMP-2) inhibitor with anti-cancer activity. It induces the inhibition of HCMV through non-classical chelate 1 (SQSTM1)/p62-Keap1-Nrf2 pathways and phosphorylation of the C-terminal domain of p62, regulating autophagy and inhibiting melanogenesis.

K67 competitively inhibits the interaction between Nrf2-ETGE and Keap1, inhibits the proliferation of HCC cells with high expression of S351 phosphorylated p62, and can be used to study cancer.

DC-LC3in-D5 is a potent and selective covalent inhibitor of LC3A/B that disrupts autophagy by covalently binding to Lys49 on LC3B (IC₅₀ = 200 nM), resulting in impaired LC3B lipidation, accumulation of the autophagy substrate p62, and a significant reduction in the formation of autophagosome vesicles.

Antitumor agent-81, a P62-RNF168 agonist with low cytotoxicity, enhances the P62-RNF168 interaction, leading to decreased RNF168-mediated H2A ubiquitination and impaired homologous recombination-mediated DNA repair. Additionally, it exhibits dose-dependent inhibition of xenograft tumor growth in mice.

Dusquetide (SGX942) TFA, a first-in-class innate defense regulator (IDR), modulates the innate immune response to pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) by interacting with p62. This compound is effective in both diminishing inflammation and enhancing the elimination of bacterial infections [1].

TRAF6 peptide, a specific TRAF6-p62 inhibitor, effectively inhibits NGF-dependent TrkA ubiquitination, showcasing strong research potential for neurological conditions including Alzheimer's disease (AD), Parkinson's, ALS, head trauma, epilepsy, and stroke [1].

TRAF6 peptide TFA, a specific inhibitor of the TRAF6-p62 interaction, significantly inhibits NGF-dependent ubiquitination of TrkA. This peptide demonstrates promising research applications in various neurological disorders, including Alzheimer's disease (AD), Parkinson's, ALS, head trauma, epilepsy, and stroke [1].

XIE62-1004 is a chemical compound that induces the interaction between p62 and LC3 by binding to the ZZ domain of p62. This interaction promotes p62 self-aggregation and its subsequent interaction with LC3 on autophagosome membranes, thereby facilitating the delivery of cargo proteins to the autophagosome for degradation. XIE62-1004 is effective both in vitro and in vivo, displaying specificity for the wild type of p62 and exhibiting its actions in a concentration- and time-dependent manner. Additionally, it induces the degradation of mutant huntingtin in vitro and can be employed in AUTAC protein degradation systems to trigger autophagy via p62 self-aggregation and LC3 interaction.

YTK-105 is a ligand targeting autophagy that binds to p62.

YOK-2204 is a ligand for the p62-ZZ domain and activates p62-dependent selective autophagy. It is also applicable in the design of AUTOTACs.

YOK-1304, an autophagy-targeting chimera (AUTOTAC), induces self-oligomerization of p62.

Fumagilin-105, an autophagy-targeting chimera (AUTOTAC), induces self-oligomerization of p62 and exhibits a DC50 of 0.7 μM against MetAP2 in HEK293 cells.

Dusquetide is a first-in-class innate defense regulator. Dusquetide displays activity in both reducing inflammation and increasing the clearance of bacterial infection.

Dihydrocelastrol is synthesized by hydrogenation of celastrol, a treterpene isolated from Chinese medicinal plant Tripterygium regelii. Dihydrocelastrol could inhibit cell proliferation and promote apoptosis through caspase-dependent way in vitro. DHCE co

CA-5f is a potent late-stage macroautophagy/autophagy inhibitor that works by inhibiting autophagosome-lysosome fusion.