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Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!2025-02-06
524 Results for "
protein degradation inducer
" in MedChemExpress (MCE) Product Catalog:
Products (524)
524 Results for "protein degradation inducer" in MCE Product Catalog:
911
911 Publications Verification
Synonyms: BafA1
Category:
Infection Microorganisms Macrolide Antibiotics Antibiotics Disease Research Anticancer Disease Research Fields
Target:
197
197 Cited Publications
Cat. No.: HY-W008923
CAS No.: 17086-28-1
Research Areas:
Infection Neurological Disease Inflammation/Immunology Cancer
Doxycycline monohydrate is an orally active highly lipophilic, tissue-permeable MMP inhibitor with broad-spectrum antibacterial activity. Doxycycline monohydrate is also a semi-synthetic antibiotic with chelating properties, which blocks bacterial protein synthesis and inhibits extracellular matrix degradation through interactions with zinc and calcium atoms. Doxycycline monohydrate also inhibits mitochondrial biogenesis, translation, and the expression of respiratory chain proteins. Doxycycline monohydrate induces apoptosis, inhibits autophagy and EMT, downregulates stem cell markers, and activates the PI3K-AKT pathway, thereby effectively inhibiting the viability and proliferation of cancer cells such as breast cancer cells. Doxycycline monohydrate also promotes the survival and self-renewal of embryonic stem cells and neural stem cells, and reduces the frequency of medium changes in culture. Doxycycline monohydrate has been applied in studies related to breast cancer, prostate cancer, bladder cancer, and other cancers .
52
52 Cited Publications
Cat. No.: HY-17439
CAS No.: 55721-31-8
Synonyms: Salinomycin sodium; Sodium salinomycin
Salinomycin sodium salt (Salinomycin sodium), an antibiotic potassium ionophore, is a potent inhibitor of Wnt/β-catenin signaling. Salinomycin sodium salt acts on the Wnt/Fzd/LRP complex, blocks Wnt-induced LRP6 phosphorylation, and causes degradation of the LRP6 protein. Salinomycin sodium salt shows selective activity against human cancer stem cells .
37
37 Cited Publications
Cat. No.: HY-16954
CAS No.: 1818885-28-7
Target:
PROTACs Epigenetic Reader Domain c-Myc Polo-like Kinase (PLK) CDK JAK STAT Pim Bcl-2 Family PAK Wnt β-catenin Caspase PARP Apoptosis Reactive Oxygen Species (ROS)
Research Areas:
ARV-825 is a BET protein PROTAC degrader that recruits cereblon, and it targets BRD2, BRD3, and BRD4 for degradation via the ubiquitin-proteasome pathway. ARV-825 downregulates c-MYC, PLK1, MYCN, CDK4/6, JAK2, pSTAT3/5, PIM1, and Bcl-xL, upregulates p21 and p27, and modulates H3K27Ac-mediated transcription, the G2/M checkpoint, the Wnt/β-catenin pathway, and amino acid transport pathways. ARV-825 induces G1 phase cell cycle arrest, caspase 3/PARP-mediated apoptosis, DNA damage, and reactive oxygen species (ROS) production, reduces mitochondrial respiration, and simultaneously inhibits cell proliferation, clonogenic growth, and cell migration. ARV-825 is used in research on gastric cancer, leukemia, neuroblastoma, and cholangiocarcinoma .
30
30 Cited Publications
Research Areas:
ARV-771 is a BET PROTAC degrader, with Kd values of 34, 4.7, 8.3, 7.6, 9.6 and 7.6 nM against BRD2 (1), BRD2 (2), BRD3 (1), BRD3 (2), BRD4 (1) and BRD4 (2) , respectively. ARV-771 inhibits the transcription of AR/AR-v7 and its downstream target genes. By degrading BRD4 protein, ARV-771 enhances the sensitivity of prostate cancer cells to ferroptosis, suppresses cancer cell viability, and induces apoptosis. ARV-771 downregulates the levels of BRD4, c-MYC and AR-V7 in tumor tissues and inhibits tumor tissue growth. ARV-771 can be used in prostate cancer-related research .
26
26 Cited Publications
Target:
Research Areas:
Cardiovascular Disease Neurological Disease Endocrinology Cancer
IU1 is a selective, reversible USP14 inhibitor with an IC50 of 4-5 μM. IU1 binds USP14’s catalytic cleft to block deubiquitinase activity. IU1 induces calpain-dependent Tau cleavage, causes ATP deficits, reduces E1~Ub thioester levels and 26S proteasome assembly. IU1 enhances 26S proteasome chymotrypsin-like activity, modulates LC3B-dependent autophagy flux, reduces cancer cell proliferation and migration, and blocks G0/G1 to S phase cell cycle transition in follicular thyroid cancer cells. IU1 activates autophagy-lysosomal and ubiquitin-proteasome pathways, triggers apoptosis, and reduces cervical cancer cell growth. IU1 enhances degradation of proteasome substrates linked to neurodegenerative disease, accelerates oxidized protein degradation, and increases oxidative stress resistance. IU1 can be used for the research of Alzheimer’s disease, follicular thyroid cancer, ischemic stroke, cervical cancer, and neurodegenerative disease .
23
23 Cited Publications
Target:
Research Areas:
KI696 is a selective KEAP1/NRF2 protein-protein interaction inhibitor with a human Kd value of 1.3 nM. KI696 acts by competitively occupying the NRF2-binding pocket of the KEAP1 Kelch domain. KI696 blocks KEAP1-mediated ubiquitination and degradation of NRF2, promotes the translocation of NRF2 to the nucleus, activates the expression of downstream antioxidant genes, increases intracellular glutathione levels, and alleviates oxidative stress-induced cell damage and inflammatory cell infiltration in the lungs. KI696 reduces ozone-induced pulmonary oxidative damage and inflammatory cell accumulation in rats, and upregulates pulmonary antioxidant genes. KI696 can be used in research related to chronic obstructive pulmonary disease, oxidative stress and inflammation .
17
17 Cited Publications
Eeyarestatin I, a potent endoplasmic reticulum-associated protein degradation (ERAD) inhibitor, is a potent protein translocation inhibitor. Eeyarestatin I inhibits Sec61 translocon. Eeyarestatin I targets the p97-associated deubiquitinating process (PAD) and inhibits atx3-dependent deubiquitination. Eeyarestatin I interferes at a step prior to proteasomal degradation. Eeyarestatin I induces cell death via the proapoptotic protein NOXA and has anticancer effects .
13
13 Cited Publications
Synonyms: AT-406 hydrochloride; Debio 1143 hydrochloride; SM-406 hydrochloride
Xevinapant (AT-406) hydrochloride is a potent and orally bioavailable Smac mimetic and an antagonist of the inhibitor of apoptosis proteins (IAPs). Xevinapant hydrochloride binds to XIAP, cIAP1, and cIAP2 proteins with Kis of 66.4, 1.9, and 5.1 nM, respectively. Xevinapant hydrochloride effectively antagonizes XIAP BIR3 protein in a cell-free functional assay, induces rapid degradation of cellular cIAP1 protein, and inhibits cancer cell growth in various human cancer cell lines. Xevinapant hydrochloride is highly effective in induction of apoptosis in xenograft tumors .
12
12 Cited Publications
Synonyms: GX15-070 Mesylate
Target:
Obatoclax Mesylate (GX15-070 Mesylate), a BH3 mimetic, is a pan-BCL-2 family proteins inhibitor with a Ki of 220 nM for BCL-2 . Obatoclax Mesylate induces autophagy-dependent cell death and targets cyclin D1 for proteasomal degradation. Obatoclax Mesylate has anti-cancer and broad-spectrum antiparasitic activity .
12
Target:
Obatoclax (GX15-070), a BH3 mimetic, is a pan-BCL-2 family proteins inhibitor with a Ki of 220 nM for BCL-2 . Obatoclax induces autophagy-dependent cell death and targets cyclin D1 for proteasomal degradation. Obatoclax has anti-cancer and broad-spectrum antiparasitic activity .
12
Target:
Research Areas:
Cardiovascular Disease Neurological Disease Inflammation/Immunology
Alvelestat (AZD9668) is an orally active, selective inhibitor of neutrophil elastase. Alvelestat reduces elastase activity, myeloperoxidase release, neutrophil recruitment and activation, and calcium phosphate precipitation; promotes smooth muscle cell colonization and collagen deposition; and inhibits the formation of neutrophil extracellular traps (NETs) as well as NET-derived neutrophil elastase activity. Alvelestat restores endothelial dysfunction, regulates antioxidant factors, improves the expression of endothelial tight junctions, reduces vascular leakage, and accelerates wound healing. Alvelestat prevents pulmonary hemorrhage, matrix protein degradation, airspace enlargement, and small airway wall remodeling; and alleviates cigarette-induced inflammatory responses. Alvelestat inhibits the growth of abdominal aortic aneurysms exacerbated by Porphyromonas gingivalis. Alvelestat can be used in research related to chronic obstructive pulmonary disease, abdominal aortic aneurysm, radiation-induced skin injury, and bronchiectasis .
11
Target:
Research Areas:
FKBP12 PROTAC dTAG-13 (dTAG-13) is a FKBP12 F36V PROTAC degrader and a PXR partial agonist. FKBP12 PROTAC dTAG-13 induces ubiquitination and proteasomal degradation of proteins tagged with FKBP12 F36V, without degrading wild-type FKBP12 or un-fused PXR. It weakly promotes the recruitment of SRC-1, strongly inhibits the interaction between NCoR and PXR, and upregulates the expression of CYP3A4 and other drug metabolism-related genes. FKBP12 PROTAC dTAG-13 is applicable to research related to breast cancer and leukemia [1] .
10
10 Cited Publications
Research Areas:
AGX51 is a pan-Id (inhibitors of DNA-binding/differentiation proteins) antagonist that disrupts ID-E protein interactions, thereby triggering ubiquitin-mediated proteasomal degradation of ID1, ID2, ID3 and ID4. AGX51 induces ROS production, G0/G1 cell cycle arrest, non-apoptotic cell death, and regulates EMT-related proteins. AGX51 reduces the proliferation, migration and myofibroblast differentiation of lung fibroblasts, alleviates pulmonary fibrosis, inhibits cancer cell viability and tumor growth, impairs neovascularization, and shows no obvious toxicity in mice. AGX51 can be used in research related to idiopathic pulmonary fibrosis, triple-negative breast cancer, breast cancer, pancreatic ductal adenocarcinoma, colorectal tumors, wet age-related macular degeneration and retinopathy of prematurity .
8
8 Cited Publications
DIF-3 is an orally active anticancer agent. DIF-3 reduces the expression levels of cyclin D1 and c-Myc by facilitating their degradation via activation of GSK-3β. DIF-3 inhibits Wnt/β-catenin signaling pathway-related proteins in cells. DIF-3 induces reactive oxygen species (ROS) and autophagy. DIF suppresses the growth of Trypanosoma. cruzi in HT1080 cells. DIF-3 exerts antitumor effects both in vitro and in vivo .
7
7 Cited Publications
Synonyms: GDC-9545; RG6171
Target:
Research Areas:
Giredestrant (GDC-9545) is an orally active, full, selective Estrogen receptor α (ERα) degrader and antagonist with a DC50 of 0.03 nM. Giredestrant promotes the degradation of ERα protein, including the ESR1 Y537S mutant ERα. Giredestrant reduces uterine wet weight in immature rats and induces a low cuboidal phenotype in their endometrial epithelium. Giredestrant induces tumor regression in both ESR1 Y537S mutant and wild-type ERα tumor models. Giredestrant can be used for the research of ER + breast cancer .
7
7 Cited Publications
IBR2 is a potent and specific RAD51 inhibitor and inhibits RAD51-mediated DNA double-strand break repair. IBR2 disrupts RAD51 multimerization, accelerates proteasome-mediated RAD51 protein degradation, inhibits cancer cell growth and induces apoptosis .
7
Research Areas:
Eragidomide (CC-90009) is a GSPT1 Molecular Glue degrader. Eragidomide exhibits antiproliferative and pro-apoptotic (apoptosis) activities against acute myeloid leukemia cells. Eragidomide recruits the CRL4CRBN E3 ubiquitin ligase complex to selectively target GSPT1 for ubiquitination and proteasomal degradation. Eragidomide reduces leukemia cell engraftment and eliminates leukemia stem cells. Eragidomide promotes the activation of the GCN1/GCN2/ATF4 pathway and the integrated stress response pathway, inhibits global protein translation, promotes preferential translation of ATF4, and induces the accumulation of ATF4, CHOP and ATF3. The response to Eragidomide is regulated by the ILF2/ILF3 heterodimer complex, the mTOR signaling pathway and the integrated stress response. Eragidomide can be used in research related to acute myeloid leukemia and relapsed/refractory acute myeloid leukemia .
6
6 Cited Publications
dTAGV-1 TFA is a selective FKBP12 F36V PORTAC degrader. dTAGV-1 TFA induces rapid degradation of FKBP12 F36V-tagged oncogenic fusion proteins, triggering collapse of downstream cellular signaling pathways, reduced proliferative capacity of cancer cells, and decreased levels of target proteins. dTAGV-1 TFA is applicable to functional validation studies of cancer and undegradable oncoproteins .
6
6 Cited Publications
dTAGV-1 hydrochloride is a selective FKBP12 F36V PORTAC degrader. dTAGV-1 hydrochloride induces rapid degradation of FKBP12 F36V-tagged oncogenic fusion proteins, triggering collapse of downstream cellular signaling pathways, reduced proliferative capacity of cancer cells, and decreased levels of target proteins. dTAGV-1 hydrochloride is applicable to functional validation studies of cancer and undegradable oncoproteins .
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Protocols
Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!A suitable model is crucial in drug screening experiments. Organs can mimic the three-dimensional functional structure of internal organs, have similar spatial organization to corresponding organs, maintain some key characteristics, and reproduce some physiological functions. They are widely used for modeling and personalized drug screening physiological functions.2025-02-06
