p62 Inhibitor

GW296115 is a multi-target inhibitor with the following IC₅₀ values against its targets: 8.4 nM for BRSK2, 21 nM for BRSK1, 1.8 μM for PDGFRβ, 5.5 nM for STK17B/DRAK2, 28 nM for DRAK1, 20 nM for PHKG1, and 89 nM for DCAMKL3. GW296115 downregulates the phosphorylation of S317 site on ULK1 and S351 site on P62, which are AMPK substrates driven by BRSK2. GW296115 does not alter the phosphorylation level of AMPK at T172, reduces nutrient deprivation-mediated Autophagy and autophagosome formation, and enhances Apoptosis. GW296115 exhibits anticancer activity against triple-negative breast cancer. GW296115 is applicable for breast cancer-related research.

XRK3F2 free base is a p62 (sequestosome-1) ZZ domain inhibitor that has specificity for the p62-ZZ domain over other p62 signaling domains. XRK3F2 free base blocks TNFα effects and upregulation in bone marrow stromal cells, and induces multiple myeloma cell apoptosis. XRK3F2 free base can be used for the research of multiple myeloma bone disease, acute myeloid leukemia, and multiple myeloma.

L-Selenocystine is a selenium-containing amino acid. L-Selenocystine has redox properties. L-Selenocystine is cytotoxic to various tumor cells and can induce the production of ROS and apoptosis. L-Selenocystine can block the Nrf2 and autophagy pathways. L-Selenocystine has anti-tumor activity.

Citronellol ((±)-Citronellol) is an orally active inducer of apoptosis. Citronellol can prevent oxidative stress, mitochondrial dysfunction, and apoptosis in the SH-SY5Y cell Parkinson's disease model induced by 6-OHDA by regulating the ROS-NO, MAPK/ERK, and PI3K/Akt signaling pathways. Citronellol can induce necroptosis in human lung cancer cells through the TNF-α pathway and accumulation of ROS. Citronellol can reduce the levels of LC-3 and p62 to regulate the autophagy pathway, inhibit oxidative stress and neuroinflammation, and thus have neuroprotective effects on Parkinson's rats. Citronellol exhibits anti-fungal activity against Trichophyton rubrum by inhibiting ergosterol synthesis.

Isoschaftoside, a C-glycosylflavonoid from Desmodium uncinatum root exudate, can inhibit the growth of germinated S. hermonthica radicles. Isoschaftoside reduces reactive oxygen species (ROS) and induces proliferation in senescent cells. Isoschaftoside activates autophagy. Isoschaftoside can be used for anti-tumor, anti-inflammatory, antioxidant, antihypertensive, hepatoprotective and nematicidal study.

2'-Aminoacetophenone is an orally active inducer of apoptosis and respiratory biomarker. 2'-Aminoacetophenone can be used to detect Pseudomonas aeruginosa infections in the lungs of cystic fibrosis patients. 2'-Aminoacetophenone can inhibit the protein levels of LC3BII and p62 in macrophages infected with pqsA or mvfR and regulate autophagy. 2'-Aminoacetophenone can disrupt mitochondrial function by inducing oxidative stress and apoptosis signaling, leading to dysfunction in mouse skeletal muscle.

PTX80 is an antagonist of p62 with an IC₅₀ value of 31.18 nM. PTX80 reduces tumor volume in an HCT116 colorectal cancer mouse xenograft model.

SKLB-D18 is an orally active ERK1/2/ERK5 inhibitor, with an IC₅₀ of 38.69 nM and a K_d of 126.9 nM against human ERK1, an IC₅₀ of 40.12 nM and a K_d of 209.8 nM against ERK2, and an IC₅₀ of 59.72 nM and a K_d of 468.2 nM against ERK5. SKLB-D18 inhibits cancer cell proliferation, induces G0/G1 cell cycle arrest and apoptosis. SKLB-D18 reduces the levels of p-ERK5, p-RSKp90, p-c-Myc and c-Myc, and upregulates the level of p-ERK1/2, thereby inhibiting the ERK1/2/5 pathway in cells. SKLB-D18 increases LC3B-II accumulation, and decreases the levels of p62, p-mTOR and p-p70S6K. SKLB-D18 elevates the levels of ROS, lipid peroxidation and free ferrous ions, reduces the levels of NCOA4 and GPX4, and induces ferritin autophagy-dependent ferroptosis in cancer cells. SKLB-D18 exhibits antitumor activity in a triple-negative breast cancer xenograft mouse model. SKLB-D18 can be used in research related to triple-negative breast cancer.

LC3in-C42 is a cell-active LC3A/B and autophagy covalent inhibitor. LC3in-C42 selectively inhibits the binding of P62 to LC3A/B in vitro and at the cellular level like D5 and can function on a lower concentration.

Citronellol (Standard) is the analytical standard of Citronellol. Citronellol (Standard) is an orally active inducer of apoptosis. Citronellol (Standard) can prevent oxidative stress, mitochondrial dysfunction, and apoptosis in the SH-SY5Y cell Parkinson's disease model induced by 6-OHDA by regulating the ROS-NO, MAPK/ERK, and PI3K/Akt signaling pathways. Citronellol (Standard) can induce necroptosis in human lung cancer cells through the TNF-α pathway and accumulation of ROS. Citronellol (Standard) can reduce the levels of LC-3 and p62 to regulate the autophagy pathway, inhibit oxidative stress and neuroinflammation, and thus have neuroprotective effects on Parkinson's rats. Citronellol (Standard) exhibits anti-fungal activity against Trichophyton rubrum by inhibiting ergosterol synthesis.

2'-Aminoacetophenone (Standard) is the analytical standard of 2'-Aminoacetophenone. This product is intended for research and analytical applications. 2'-Aminoacetophenone is an orally active inducer of apoptosis and respiratory biomarker. 2'-Aminoacetophenone can be used to detect Pseudomonas aeruginosa infections in the lungs of cystic fibrosis patients. 2'-Aminoacetophenone can inhibit the protein levels of LC3BII and p62 in macrophages infected with pqsA or mvfR and regulate autophagy. 2'-Aminoacetophenone can disrupt mitochondrial function by inducing oxidative stress and apoptosis signaling, leading to dysfunction in mouse skeletal muscle.

Atiprimod (Azaspirane) is a STAT3 inhibitor with antitumor, anti-inflammatory, and anti-angiogenic activities. Atiprimod blocks the signaling pathways of IL-6 and VEGF by inhibiting the phosphorylation of signal transducer and activator of STAT3. Atiprimod blocks the JAK-STAT signaling pathway by inhibiting the phosphorylation of JAK2 and JAK3. Atiprimod also inhibits cell proliferation, induces cell cycle arrest, and induces autophagy and apoptosis. Atiprimod triggers persistent ER stress-mediated apoptosis in breast cancer cells by activating the PERK/eIF2α/ATF4/CHOP axis and inhibiting the nuclear translocation of STAT3/NF-κB. Atiprimod shows great anti-tumor activities in tumor xenograft mouse models. Atiprimod can be used for the study of pituitary adenoma, breast cancer, multiple myeloma and acute myeloid leukemia (AML).

Atiprimod (Azaspirane) (dimaleate) is a STAT3 inhibitor with antitumor, anti-inflammatory, and anti-angiogenic activities. Atiprimod blocks the signaling pathways of IL-6 and VEGF by inhibiting the phosphorylation of signal transducer and activator of STAT3. Atiprimod blocks the JAK-STAT signaling pathway by inhibiting the phosphorylation of JAK2 and JAK3. Atiprimod also inhibits cell proliferation, induces cell cycle arrest, and induces autophagy and apoptosis. Atiprimod triggers persistent ER stress-mediated apoptosis in breast cancer cells by activating the PERK/eIF2α/ATF4/CHOP axis and inhibiting the nuclear translocation of STAT3/NF-κB. Atiprimod shows great anti-tumor activities in tumor xenograft mouse models. Atiprimod can be used for the study of pituitary adenoma, breast cancer, multiple myeloma and acute myeloid leukemia (AML).

TrxR-IN-2 is a thioredoxin reductase (TrxR) inhibitor. TrxR-IN-2 increases reactive oxidative species (ROS) levels and decreases mitochondrial transmembrane potential levels. TrxR-IN-2 triggers DNA damage via H2AX regulation, and induces autophagy via LC3, beclin-1, and p62 regulation. TrxR-IN-2 can be used for the research of drug-resistant hepatocellular carcinoma^[1].

Isoschaftoside (Standard) is the analytical standard of Isoschaftoside. This product is intended for research and analytical applications. Isoschaftoside, a C-glycosylflavonoid from Desmodium uncinatum root exudate, can inhibit growth of germinated S. hermonthica radicles. Isoschaftoside reduces reactive oxygen species (ROS) and induces proliferation in senescent cells. Isoschaftoside activates autophagy. Isoschaftoside can be used for anti-tumor, anti-inflammatory, antioxidant, antihypertensive, hepatoprotective and nematicidal study.

EGFR/tubulin-IN-1 (Compound 26) is a dual-target inhibitor of EGFR and tubulin. EGFR/tubulin-IN-1 significantly reduces the levels of p-EGFR, p-AKT, and p-ERK in cells, disrupting the microtubule structure of the cells. EGFR/tubulin-IN-1 significantly inhibits the proliferation of H1975 cells and significantly blocks the cells in the G2/M phase. EGFR/tubulin-IN-1 induces the expression of autophagy markers LC3B-II and Beclin-1, while down-regulating the expression of p62. EGFR/tubulin-IN-1 induces ferroptosis, with increased ROS content and depletion of glutathione (GSH). EGFR/tubulin-IN-1 inhibits epithelial-mesenchymal transition (EMT) and tumor metastasis. EGFR/tubulin-IN-1 has a significant tumor-suppressing effect in the H1975 transplanted tumor nude mouse model. EGFR/tubulin-IN-1 can be used for the study of non-small cell lung cancer.

VCP/p97 IN-3 is a VCP/p97 allosteric inhibitor. VCP/p97 IN-3 shows the inhibitory activity against the VCP proteins with an IC₅₀ of 9 nM and the mutant VCP proteins with IC₅₀ of 12 nM (N660K) and 19 nM (V474A/D649A). VCP/p97 IN-3 increases K48-linked ubiquitination and the level of cleaved caspase-3. VCP/p97 IN-3 activates ER-stress and the UPR. VCP/p97 IN-3 inhibits tumor growth in RPMI-8226 cell subcutaneous xenograft mouse models. VCP/p97 IN-3 can be used for the study of multiple myeloma.

ICSN3250 hydrochloride is a halitulin analogue and a mTORC1 inhibitor. ICSN3250 hydrochloride directly binds to mTOR's FRB domain and displaces phosphatidic acid (PA), reversing mTORC1 activation. ICSN3250 hydrochloride shows high cytotoxicity in cancer cells (nanomolar concentration) through a caspase-independent cell death mechanism. ICSN3250 hydrochloride specifically inhibits the mTORC1 pathway, inducing autophagy and G0-G1 cell-cycle arrest in cancer cells. ICSN3250 hydrochloride can be used for the study of cancer .

CDC25A/NF-κB-IN-1 is an effective dual-target inhibitor of CDC25A and NF-κB, and is a prodrug of Pt(IV). CDC25A/NF-κB-IN-1 has anticancer activity and low cytotoxicity to normal cells. CDC25A/NF-κB-IN-1 can trigger a variety of anticancer mechanisms, including S phase cell cycle arrest, mitochondrial endogenous apoptosis, endoplasmic reticulum stress, autophagy-dependent ferroptosis. CDC25A/NF-κB-IN-1 has good safety and can be used for ovarian cancer research.

Nur77 modulator 3 is a Nur77 modulator. Nur77 modulator 3 induces Nur77 expression, inhibits hepatic stellate cells (HSCs) activation, and reduces extracellular matrix (ECM) deposition. Nur77 modulator 3 enhances Nur77-denpendent autophagic flux and significantly inhibits the mTORC1 signaling pathway. Nur77 modulator 3 ameliorates HSCs activation, inflammation and hepatic fibrosis in vivo.