404 Results for "

Protein Oxidation

" in MedChemExpress (MCE) Product Catalog:
Products (404)

404 Results for "Protein Oxidation" in MCE Product Catalog:

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Cat. No.: HY-143346
CAS No.: 2361138-33-0
Purity:  98.73%
CCW16 is a non-selective cysteine-reactive covalent ligand and an RNF4 E3 ubiquitin ligase recruiter with an IC50 of 1.8 μM against human RNF4[. CCW16 covalently modifies accessible cysteine residues on RNF4, PRDX1, PRDX2, and PRDX6, attenuating the peroxide-scavenging activity of peroxiredoxins. CCW16 induces oxidative stress through upregulation of HMOX1 and NRF2, and triggers ferroptosis via lipid peroxidation and ROS signaling pathways in an RNF4-independent manner. CCW16 serves as an RNF4-recruiting moiety; it does not induce RNF4 degradation when used alone and can be used to synthesize protein degraders, such as the PROTAC compound CCW 28-3 (HY-156774). CCW16 can be used for research on acute myeloid leukemia and hepatocellular carcinoma .
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Cat. No.: HY-16658BG
CAS No.: 161401-82-7
Z-VAD-FMK is a pan-caspase inhibitor and also an ICE-like protease inhibitor, which inhibits apoptosis by preventing the processing of CPP32 to its active form. Z-VAD-FMK sensitivity varies primarily due to differential expression of receptor-interacting protein 1 (RIP1). Z-VAD-FMK limits the cryopreservation-induced apoptosis by reducing caspase-3 activity of in vitro produced bovine embryos. Z-VAD-FMK is immunosuppressive in vitro and inhibits T cell proliferation without blocking the processing of caspase-8 and caspase-3. Z-VAD-FMK leads to a decrease in intracellular glutathione (GSH) with a concomitant increase in reactive oxygen species (ROS) levels in activated T cells. Z-VAD-FMK is due to oxidative stress via the depletion of GSH. Z-VAD-FMK can be used for the study of acute pancreatitis .
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Cat. No.: HY-175521
HIF-1α-IN-8 is an orally active HIF-1α inhibitor, with an IC50 of 2.02 μM. HIF-1α-IN-8 significantly suppresses the expression of inflammation factors of IL-6 and NO, reduces hypoxia-induced ROS production and apoptosis in C8-D1A cells. HIF-1α-IN-8 inhibits HIF-1α/IKKα/NF-κB signaling pathway and reduces the expression of blood-brain barrier permeability-related proteins. HIF-1α-IN-8 reduces brain water content and oxidative stress level in mice with high altitude cerebral edema (HACE) model. HIF-1α-IN-8 can be used for the study of high altitude cerebral edema (HACE) .
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Cat. No.: HY-78036
CAS No.: 498-24-8
Synonyms: Citronic acid; Methylfumaric acid
Mesaconic acid (Citronic acid; Methylfumaric acid) is an orally active anti-inflammatory and antioxidant agent. Mesaconic acid reduces the level of NF-κB in colon tissues, downregulates the expression of Keap1 and Bax, upregulates the expression of Nrf2 and Bcl2, and decreases the expression of Caspase-1. Mesaconic acid reduces the levels of NLRP3, ASC and Casp-1 in colon, liver and kidney tissues. Mesaconic acid reduces pro-inflammatory cytokine levels, increases the level of the anti-inflammatory cytokine IL-10, elevates NAD + levels, regulates oxidative stress markers and antioxidant enzyme levels, and upregulates intestinal barrier proteins in colon, liver and kidney tissues. Mesaconic acid increases the abundance of beneficial gut bacteria and reduces the abundance of harmful gut bacteria in rapidly aging mice, and exhibits anti-aging properties. Mesaconic acid acts as a flame retardant and serves as a competitive inhibitor of fumarate reduction. Mesaconic acid can be used in the research of aging-related inflammation .
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Cat. No.: HY-D3427
CAS No.: 3100316-45-5
T-sCPY-s500R-H is a NADPH-based FRET ratiometric biosensor probe. T-sCPY-s500R-H forms a 1:1 FRET pair upon binding to the eDHFR-HaloTag fusion protein through conjugation of the donor s500R (green fluorescence) and the acceptor sCPY (red fluorescence) with the HaloTag ligand and the eDHFR ligand (TMP), respectively; NADPH binding to eDHFR induces a conformational change that converts sCPY from a colorless spirolactam form to a red fluorescent form, enabling quantification of NADPH levels through the ratio of red/green fluorescence intensity (Ex = 488 or 490 nm; green channel Em = 500-580 nm; red channel Em = 600-700 nm). T-sCPY-s500R-H is applicable to research in fields such as cell metabolism studies, oxidative stress and NADPH homeostasis analysis, tumor metabolism, and NADPH-modulating drug screening .
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Cat. No.: HY-NP143
CAS No.: 93928-24-6
Nerve Growth Factor 2.5S,murine submaxillary gland is a neurotrophic polypeptide and protein growth factor isolated from murine submaxillary glands. Nerve Growth Factor 2.5S,murine submaxillary gland increases the survival rate, phagocytic capacity and superoxide anion production level of mouse cells. Nerve Growth Factor 2.5S,murine submaxillary gland acts through cell membrane surface receptors to mediate the differentiation and maintenance of adrenergic neurons in the sympathetic nervous system. Nerve Growth Factor 2.5S,murine submaxillary gland loses its activity and undergoes dimer dissociation due to oxidation; it remains active after modification of specific tryptophan residues, while its tyrosine residues are not essential for activity. Nerve Growth Factor 2.5S,murine submaxillary gland may play a role in the inflammatory process .
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Cat. No.: HY-L045
4,317 compounds

Oxygen homeostasis regulation is the most fundamental cellular process for adjusting physiological oxygen variations, and its irregularity leads to various human diseases, including cancer. Hypoxia is closely associated with cancer development, and hypoxia/oxygen-sensing signaling plays critical roles in the modulation of cancer progression.

Hypoxia-inducible factor 1 (HIF-1) is a transcription factor that functions as a master regulator of oxygen homeostasis. A variety of HF-1 target genes have been identified thus far which encode proteins that play key roles in critical developmental and physiological processes including angiogenesis/vascular remodeling, erythropoiesis, glucose transport, glycolysis, iron transport, and cell proliferation/survival.

HIF-1 is a heterodimeric transcription factor consisting of a constitutively expressed β-subunit and an oxygen-regulated α-subunit. The unique feature of HIF-1 is the regulation of HIF-1α expression and activity based upon the cellular O2 concentration. Under normoxic conditions, hydroxylation of HIF-1α on these different proline residues is essential for HIF proteolytic degradation by promoting interaction with the von Hippel-Lindau tumor-suppressor protein (pVHL) through hydrogen bonding to the hydroxyproline-binding pocket in the pVHL β-domain. As oxygen levels decrease, hydroxylation of HIF decreases; HIF-1α then no longer binds pVHL, and becomes stabilized, allowing more of the protein to translocate to the cell’s nucleus, where it acts as a transcription factor, upregulating (often within minutes) the production of proteins that stimulate blood perfusion in tissues and thus tissue oxygenation.

MCE offers a unique collection of 4,317 oxygen sensing related compounds targeting HIF/HIF Prolyl-Hydroxylase, MAPK/ERK, PI3K/AKT signaling pathways, etc. MCE Oxygen Sensing Compound Library is a useful tool to study hypoxia, oxidative stress and discover new anti-cancer drugs.

Cat. No.: HY-160906
CAS No.: 32607-79-7
Synonyms: GSSSG
Glutathione trisulfide (GSSSG) is an orally active, blood-brain barrier permeable neuroprotective agent. Glutathione trisulfide inactivates intracellular tyrosinase, regulates the expression of Cars2, Cbs, MITF and TYR, inhibits α-MSH (HY-P0252)-induced melanogenesis, and restores intracellular persulfide levels reduced by α-MSH. Glutathione trisulfide scavenges free radicals, quenches ROS, reduces Paclitaxel (HY-B0015)-induced superoxide production, upregulates the expression of antioxidant protein genes, and inhibits oxidative stress-induced cell death. Glutathione trisulfide promotes ERK1/2 activation, prevents NF-κB p65 activation, inhibits TAK1 phosphorylation, reduces pro-inflammatory cytokine expression, and blocks microglial activation. Glutathione trisulfide can be used in research related to dry age-related macular degeneration, inflammation-associated eye diseases, Alzheimer's disease, Parkinson's disease, etc.
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Cat. No.: HY-160906A
Synonyms: GSSSG TFA
Glutathione trisulfide TFA (GSSSG TFA) is an orally active, blood-brain barrier permeable neuroprotective agent. Glutathione trisulfide TFA inactivates intracellular tyrosinase, regulates the expression of Cars2, Cbs, MITF and TYR, inhibits α-MSH (HY-P0252)-induced melanogenesis, and restores intracellular persulfide levels reduced by α-MSH. Glutathione trisulfide TFA scavenges free radicals, quenches ROS, reduces Paclitaxel (HY-B0015)-induced superoxide production, upregulates the expression of antioxidant protein genes, and inhibits oxidative stress-induced cell death. Glutathione trisulfide TFA promotes ERK1/2 activation, prevents NF-κB p65 activation, inhibits TAK1 phosphorylation, reduces pro-inflammatory cytokine expression, and blocks microglial activation. Glutathione trisulfide TFA can be used in research related to dry age-related macular degeneration, inflammation-associated eye diseases, Alzheimer's disease, Parkinson's disease, etc.
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Cat. No.: HY-178448
EGFR-IN-178 is an orally active EGFR mutant inhibitor, exhibits highly selective inhibitory activity against mutants of the EGFR enzyme, including Del19 (IC50 = 3.4 nM), L858R/T790 M (IC50 = 2.9 nM), and Del19/T790 M (IC50 = 2.5 nM). EGFR-IN-178 has good activity against JAK2 (IC50 = 55.6 nM) and JAK3 (IC50 = 46.1 nM) kinases. EGFR-IN-178 can increase cellular lipid oxide MDA, meanwhile decrease GSH content, causing ferroptosis in cancer cells. EGFR-IN-178 promotes apoptosis by increasing cleaved caspase-3 expression. EGFR-IN-178 can inhibit the phosphorylation of EGFR protein and decrease the active form p-JAK2 for JAK2, induce an increase in intracellular ROS. EGFR-IN-178 can be used for the study of non-small cell lung cancer (NSCLC) .
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Cat. No.: HY-78036R
CAS No.: 498-24-8
Synonyms: Citronic acid (Standard); Methylfumaric acid (Standard)
Mesaconic acid (Standard) is the analytical standard of Mesaconic acid. This product is intended for research and analytical applications. Mesaconic acid (Citronic acid; Methylfumaric acid) is an orally active anti-inflammatory and antioxidant agent. Mesaconic acid reduces the level of NF-κB in colon tissues, downregulates the expression of Keap1 and Bax, upregulates the expression of Nrf2 and Bcl2, and decreases the expression of Caspase-1. Mesaconic acid reduces the levels of NLRP3, ASC and Casp-1 in colon, liver and kidney tissues. Mesaconic acid reduces pro-inflammatory cytokine levels, increases the level of the anti-inflammatory cytokine IL-10, elevates NAD + levels, regulates oxidative stress markers and antioxidant enzyme levels, and upregulates intestinal barrier proteins in colon, liver and kidney tissues. Mesaconic acid increases the abundance of beneficial gut bacteria and reduces the abundance of harmful gut bacteria in rapidly aging mice, and exhibits anti-aging properties. Mesaconic acid acts as a flame retardant and serves as a competitive inhibitor of fumarate reduction. Mesaconic acid can be used in the research of aging-related inflammation .
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Cat. No.: HY-N0427
CAS No.: 6873-13-8
Phellodendrine is an orally active plant alkaloid. Phellodendrine inhibits the proliferation of KRAS-mutated pancreatic cancer cells by suppressing macropinocytosis and glutamine metabolism, inducing ROS accumulation and mitochondrial apoptosis. Phellodendrine promotes autophagy by activating the AMPK/mTOR pathway, alleviating intestinal damage in ulcerative colitis. Phellodendrine can alleviate gouty arthritis by inhibiting the IL-6/STAT3 signaling pathway. Phellodendrine suppresses allergic reactions by altering the conformation of MRGPRB3/MRGPRX2 protein, thereby inhibiting the activation of PKC and subsequent downstream MAPK and NF-κB signaling. Phellodendrine inhibits the AKT/NF-κB pathway and down-regulates the expression of COX-2, thereby protecting zebrafish embryos from oxidative stress. Phellodendrine has an anti-major depressive disorder (MDD) effect by down-regulating CHRM1, HTR1A, and the PI3K/Akt signaling pathway .
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Cat. No.: HY-N0735R
CAS No.: 104112-82-5
Phellodendrine chloride (Standard) is the analytical standard of Phellodendrine chloride (HY-N0735). Phellodendrine chloride is an orally active plant alkaloid. Phellodendrine chloride inhibits the proliferation of KRAS-mutated pancreatic cancer cells by suppressing macropinocytosis and glutamine metabolism, inducing ROS accumulation and mitochondrial apoptosis. Phellodendrine chloride promotes autophagy by activating the AMPK/mTOR pathway, alleviating intestinal damage in ulcerative colitis. Phellodendrine chloride can alleviate gouty arthritis by inhibiting the IL-6/STAT3 signaling pathway. Phellodendrine chloride suppresses allergic reactions by altering the conformation of MRGPRB3/MRGPRX2 protein, thereby inhibiting the activation of PKC and subsequent downstream MAPK and NF-κB signaling. Phellodendrine chloride inhibits the AKT/NF-κB pathway and down-regulates the expression of COX-2, thereby protecting zebrafish embryos from oxidative stress. Phellodendrine chloride has an anti-major depressive disorder (MDD) effect by down-regulating CHRM1, HTR1A, and the PI3K/Akt signaling pathway.
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Cat. No.: HY-N12060
CAS No.: 90045-36-6
Ginkgo biloba extract is a natural product that can be isolated from Ginkgo biloba leaves . Ginkgo biloba extract alleviates oxidative stress-induced neuronal apoptosis (Apoptosis) by stabilizing mitochondrial function, regulating Bcl-2 family proteins and inhibiting caspase activation. Ginkgo biloba extract alleviates testicular injury by upregulating SKP2 and inhibiting Beclin1-independent autophagy (Autophagy) . Ginkgo biloba extract alleviates various types of neuronal damage in animal models. Ginkgo biloba extract reduces behavioral sensitization in rats. Ginkgo biloba extract counteracts Aβ-induced neurotoxicity by blocking a series of Aβ-triggered events, including glucose uptake, ROS accumulation, AKT activation, mitochondrial dysfunction, JNK and ERK 1/2 pathways, and apoptosis, and also interferes with the formation of Aβ oligomers. Ginkgo biloba extract is applicable to research related to cerebral hypoperfusion, testicular injury, Alzheimer's disease, Parkinson's disease, multi-infarct dementia, stroke, traumatic brain injury and amyotrophic lateral sclerosis .
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Cat. No.: HY-122895A
CAS No.: 2285446-67-3
Purity:  98.09%
Target:  

PDI Apoptosis

연구분야:  

Cancer

(E/Z)-E64FC26 is a mixture of the stereoisomers E-E64FC26 and Z-E64FC26, in which E-E64FC26 is the active component and acts as a potent PDI inhibitor. The IC50 values of E64FC26 (E-E64FC26) for PDIA1, PDIA3, PDIA4, TXNDC5, and PDIA6 are 0.6, 4.8, 33.1, 12.1, and 5.7 μM, respectively. By inhibiting PDI, (E/Z)-E64FC26 causes massive intracellular accumulation of misfolded polyubiquitinated proteins, thereby triggering strong endoplasmic reticulum stress and oxidative stress responses, which in turn induce apoptosis. (E/Z)-E64FC26 is used in research on multiple myeloma, ovarian cancer, and breast cancer .
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Cat. No.: HY-142026
CAS No.: 142449-89-6
Synonyms: (+)-Vitisin A
Vitisin A ((+)-Vitisin A) is an orally active natural product with multiple pharmacological activities including anti-inflammatory, anti-tumor, anti-oxidant, anti-pathogenic microorganism, hypoglycemic and lipid-regulating, anti-osteoporotic, neuroprotective and cardiovascular protective effects. Vitisin A exhibits inhibitory effects on human AChE and MAO-B with IC50 values of 1.29 µM and 4.94 µM, respectively. Vitisin A inhibits the ERK, MAPK, NF-κB, STAT1, HMGCR and TRAF6 pathways, downregulates the related phosphorylation and protein expression, while activates the Nrf2/HO-1 pathway and upregulates p21 expression. Vitisin A induces tumor cell apoptosis and cell cycle arrest, inhibits adipogenesis and lipid accumulation, while alleviates oxidative stress, suppresses inflammatory responses, blocks hepatic fibrosis, Cuproptosis and cholesterol synthesis, and increases the expression levels of central BDNF and TrkB. Vitisin A can be used in the research of tumors, infectious diseases, metabolic diseases, bone and joint diseases, liver diseases, skin injuries, as well as neurodegenerative and cognitive dysfunction-related diseases .
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Cat. No.: HY-153932
CAS No.: 2550399-06-7
연구분야:  

Infection Cancer

NR-7h is a selective p38α/p38β MAPK PROTAC degrader with multiple activities including anti-leishmanial, anti-malarial, and anti-Mayaro virus properties. NR-7h induces specific degradation of p38α/p38β isoforms and p38-MAPK via the ubiquitin-proteasome system. NR-7h reduces the load of Leishmania donovani, modulates the cytokine profile toward a pro-inflammatory phenotype, and enhances the oxidative burst of macrophages. NR-7h inhibits the growth of Plasmodium falciparum in human red blood cells and merozoite invasion. NR-7h reduces the replication of Mayaro virus and the expression of E1 protein in primary human dermal fibroblasts. NR-7h can be used in studies related to parasitic infections, viral infections, and breast cancer .
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Cat. No.: HY-16658BR
CAS No.: 161401-82-7
Synonyms: Z-VAD(OH)-FMK (Standard)
Z-VAD-FMK (Standard) is the analytical standard of Z-VAD-FMK (HY-16658B). This product is intended for research and analytical applications. Z-VAD-FMK is a pan-caspase inhibitor and also an ICE-like protease inhibitor, which inhibits apoptosis by preventing the processing of CPP32 to its active form. Z-VAD-FMK sensitivity varies primarily due to differential expression of receptor-interacting protein 1 (RIP1). Z-VAD-FMK limits the cryopreservation-induced apoptosis by reducing caspase-3 activity of in vitro produced bovine embryos. Z-VAD-FMK is immunosuppressive in vitro and inhibits T cell proliferation without blocKing the processing of caspase-8 and caspase-3. Z-VAD-FMK leads to a decrease in intracellular glutathione (GSH) with a concomitant increase in reactive oxygen species (ROS) levels in activated T cells. Z-VAD-FMK is due to oxidative stress via the depletion of GSH. Z-VAD-FMK can be used for the study of acute pancreatitis .
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Cat. No.: HY-171705
CAS No.: 1478585-60-2
KMS99220 is an orally active, blood-brain barrier-permeable activator of the Nrf2 inhibitory protein Keap-1. KMS99220 enhances the activity of AMPK, activates the Nrf2 signaling pathway, and reduces the phosphorylation of IκB, nuclear translocation of NFκB, as well as the phosphorylation levels of JNK, IKK and p38 MAPK via HO-1. KMS99220 binds to Keap1 to trigger the nuclear translocation of Nrf2, induces the expression of HO-1, NQO1, GCLC, GCLM and proteasome subunits; enhances proteasomal enzymatic activity; inhibits iNOS expression, nitric oxide production and IL-1β generation; attenuates microglial activation; reduces α-synuclein aggregation; and prevents dopaminergic neuron degeneration and motor dysfunction. KMS99220 prevents the degeneration of dopaminergic neurons in the substantia nigra, induces the expression of Nrf2 downstream target genes, and effectively ameliorates associated motor dysfunction in a mouse model of Parkinson's disease. KMS99220 is applicable to research related to Parkinson's disease .
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Cat. No.: HY-N20682
CAS No.: 2866266-56-8
1-Hydroxy-4αH-1,10-secoeudesma-5(6),10(14),11(13)-trien-12,8β-olide is a neuroprotective agent. 1-Hydroxy-4αH-1,10-secoeudesma-5(6),10(14),11(13)-trien-12,8β-olide reduces the protein expression levels of iNOS and COX-2, blocks the DNA-binding activity of NF-κB, and inhibits nitric oxide production. 1-Hydroxy-4αH-1,10-secoeudesma-5(6),10(14),11(13)-trien-12,8β-olide promotes the polarization of microglia to the M2 phenotype by inducing the production of Arg-1, and alleviates cell damage induced by H2O2 and 6-Hydroxydopamine (HY-B1081) .
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