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Results for "

lipid peroxidation accumulation

" in MedChemExpress (MCE) Product Catalog:

61

Inhibitors & Agonists

2

Peptides

15

Natural
Products

15

Isotope-Labeled Compounds

1

Oligonucleotides

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-N0717
    L-Valine
    5 Publications Verification

    (S)-Valine

    		 Bacterial Arginase Akt Infection
    L-Valine ((S)-Valine) is a nonlinear semiorganic material. L-Valine causes lipid peroxidation and accumulation of malondialdehyde (MDA), exhibits inhibitory activity against cyanobacteria. L-Valine inhibits multidrug-resistant bacteria through activation of PI3K/Akt signaling pathway and inhibition of arginase .
    L-Valine
  • HY-113402
    Gamma-glutamylcysteine
    4 Publications Verification

    γ-Glu-Cys

    		 Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
    Gamma-glutamylcysteine
  • HY-I1124
    L-Valine-d8
    1 Publications Verification

    L-VALINE-2,3,4,4,4,5,5,5-d8

    		 Isotope-Labeled Compounds Arginase Akt Bacterial Infection
    L-Valine-d8 is a deuterated form of L-Valine (HY-N0717). L-Valine ((S)-Valine) is a nonlinear semiorganic material. L-Valine causes lipid peroxidation and accumulation of malondialdehyde (MDA), exhibits inhibitory activity against cyanobacteria. L-Valine inhibits multidrug-resistant bacteria through activation of PI3K/Akt signaling pathway and inhibition of arginase .
    L-Valine-d8
  • HY-113402A
    Gamma-glutamylcysteine TFA
    4 Publications Verification

    γ-Glu-Cys TFA

    		 Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
    Gamma-glutamylcysteine TFA
  • HY-N0468
    Rebaudioside D
    1 Publications Verification

    		 FXR Acetyl-CoA Carboxylase Metabolic Disease
    Rebaudioside D is an orally active sweetener that targets and activates FXR, modulates Acetyl-CoA Carboxylase, and inhibits 3-hydroxy-3-methylglutaryl-CoA reductase. Rebaudioside D regulates bile acid homeostasis and lipid metabolism, reduces the synthesis rates of fatty acids and cholesterol, and exerts multiple effects including anti-adipogenesis, hepatoprotection, anti-steatosis, gut microbiota modulation, enhancement of secondary bile acid metabolism, anti-endotoxin activity, regulation of bile acid transport, and inhibition of bile acid efflux. Rebaudioside D also reduces body weight gain, visceral fat accumulation, hepatic triglyceride and cholesterol accumulation, hepatic lipid peroxidation, and decreases the circulating level of lipopolysaccharide-binding protein. Rebaudioside D additionally enhances the secondary bile acid metabolic pathway of intestinal bacteria, upregulates the gene expression of ileal organic solute transporter α, and downregulates the gene expression of hepatic bile salt export pump. Rebaudioside D does not affect glucose homeostasis, alter total caloric intake or fecal energy excretion, induce weight gain, exacerbate obesity, promote hepatic steatosis, impair brown adipose tissue function, nor change skeletal muscle metabolism-related proteins. Rebaudioside D can be used in diet-induced obesity and obesity-related research .
    Rebaudioside D
  • HY-N1990
    Gypenoside XLIX
    2 Publications Verification

    		 PPAR Sirtuin Keap1-Nrf2 Toll-like Receptor (TLR) NF-κB Reactive Oxygen Species (ROS) NOD-like Receptor (NLR) Apoptosis Pyroptosis Autophagy Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    Gypenoside XLIX is a multifunctional bioactive compound that can be isolated from Gynostemma pentaphyllum, with a Ka value of 1.58 μM for its binding to SIRT1. Gypenoside XLIX acts as a PPAR-α agonist. It inhibits the activation of TLR4-mediated NF-κB signaling pathway by activating the Sirt1/Nrf2 signaling pathway, reduces ROS accumulation, and alleviates hepatic inflammatory injury in mice with sepsis-induced liver disease. Gypenoside XLIX targets SIRT1 to block YAP-NLRP3 activation and improve sepsis-induced cardiomyopathy. Gypenoside XLIX inhibits apoptosis (Apoptosis), pyroptosis (Pyroptosis), autophagy (Autophagy), lipid peroxidation, pro-inflammatory cytokines and anti-inflammatory cytokines. Gypenoside XLIX alleviates sepsis-induced splenic injury by inhibiting inflammation and oxidative stress, and mitigates sepsis-associated encephalopathy by targeting PPAR-α. Gypenoside XLIX prevents acute kidney injury by inhibiting IGFBP7/IGF1R-mediated programmed cell death and inflammation. Gypenoside XLIX inhibits the expression and activity of vascular cell adhesion molecule-1 in cytokine-induced human endothelial cells. Gypenoside XLIX is applicable to research related to acute liver injury, lung injury, cardiomyopathy, acute splenic injury, sepsis-associated encephalopathy, acute kidney injury, atherosclerosis and chronic inflammation .
    Gypenoside XLIX
  • HY-N0717S6
    L-Valine-13C5

    (S)-Valine-13C5

    		 Isotope-Labeled Compounds Arginase Akt Bacterial Infection
    L-Valine- 13C5 ((S)-Valine- 13C5) is the 13C-labeled L-Valine (HY-N0717). L-Valine ((S)-Valine) is a nonlinear semiorganic material. L-Valine causes lipid peroxidation and accumulation of malondialdehyde (MDA), exhibits inhibitory activity against cyanobacteria. L-Valine inhibits multidrug-resistant bacteria through activation of PI3K/Akt signaling pathway and inhibition of arginase .
    L-Valine-13C5
  • HY-N6929
    Angelic acid
    1 Publications Verification

    		 Ferroptosis Keap1-Nrf2 Reactive Oxygen Species (ROS) Neurological Disease Cancer
    Angelic acid is a ferroptosis inducer, targeting NRF2 degradation. Angelic acid binds to NRF2 protein and promotes NRF2 degradation via ubiquitination-proteasome pathway, relieves the inhibitory effect of NRF2 on oxidative stress and lipid peroxidation. Then, Angelic acid induces ferroptosis in tumor cells. Angelic acid can enhance the accumulation of intracellular reactive oxygen species (ROS), upregulate ferroptosis-related markers CHAC1 and PTGS2, and synergize with ferroptosis inducers to enhance anti-tumor effects. Angelic acid also has the activity of scavenging UVA-induced ROS in vitro, inhibiting skin fibroblast senescence and extracellular matrix degradation. Angelic Acid helps wound healing with sedative activity .
    Angelic acid
  • HY-161929
    GPX4 activator 2

    		Glutathione Peroxidase Ferroptosis Cardiovascular Disease
    GPX4 activator 2 is a GPX4 activator with a Ka value of 0.426 μM for human GPX4. GPX4 activator 2 reduces lipid hydroperoxide levels, prevents lipid peroxide accumulation, and inhibits ferroptosis. GPX4 activator 2 rescues cell death induced by Erastin (HY-15763). GPX4 activator 2 exerts cardioprotective effects in a mouse model of doxorubicin (HY-15142A)-induced myocardial injury .
    GPX4 activator 2
  • HY-N0717R
    L-Valine (Standard)

    (S)-Valine (Standard)

    		 Reference Standards Arginase Akt Bacterial Infection
    L-Valine (Standard) ((S)-Valine (Standard)) is the analytical standard of L-Valine (HY-N0717). This product is intended for research and analytical applications. L-Valine ((S)-Valine) is a nonlinear semiorganic material. L-Valine causes lipid peroxidation and accumulation of malondialdehyde (MDA), exhibits inhibitory activity against cyanobacteria. L-Valine inhibits multidrug-resistant bacteria through activation of PI3K/Akt signaling pathway and inhibition of arginase .
    L-Valine (Standard)
  • HY-P1723
    Spexin
    2 Publications Verification

    Neuropeptide Q

    		 Neuropeptide Y Receptor Apoptosis Ferroptosis Autophagy Cardiovascular Disease Neurological Disease
    Spexin (Neuropeptide Q) is a selective agonist of galanin receptors GAL2 and GAL3, and is a conserved peptide that functions as a neurotransmitter/neuromodulator and endocrine factor. Spexin can function through both central and peripheral actions. Spexin upregulates Beclin 1 to inhibit ferroptosis induced by excessive autophagy, reduces the uptake of long-chain fatty acids by adipocytes, and regulates energy metabolism by increasing lipid oxidation (e.g., reducing the respiratory exchange ratio in rodents). Spexin improves cardiac function in the Doxorubicin hydrochloride (HY-15142)-induced cardiotoxicity model, protects mitochondrial membrane potential, and reduces iron accumulation and lipid peroxidation. Spexin can be used to study obesity and its related metabolic disorders, cardiovascular diseases (e.g., cardioprotection), and side effects of tumor chemotherapy .
    Spexin
  • HY-146682
    KS100

    		Aldehyde Dehydrogenase (ALDH) Apoptosis Cancer
    KS100 is a potent ALDH inhibitor with IC50s of 230, 1542, 193 nM for ALDH1A1, ALDH2, and ALDH3A1, respectively. KS100 shows antiproliferative and anticancer effects with low low toxic. KS100 significantly increases ROS activity, lipid peroxidation and toxic aldehyde accumulation. KS10600 induces apoptosis and cell cycle arrest at the G2/M phase .
    KS100
  • HY-161928
    GPX4 activator 1

    		Glutathione Peroxidase Ferroptosis Cancer
    GPX4 activator 1 (Compound A9) is a allosteric activator of GPX4 (Kd = 5.86 μM, EC50 = 19.19 μM). GPX4 activator 1 can selectively act on ferroptosis and prevent the accumulation of intracellular lipid peroxides caused by ferroptosis inducers .
    GPX4 activator 1
  • HY-N0717S4
    L-Valine-1-13C

    (S)-Valine-1-13C

    		 Isotope-Labeled Compounds Arginase Akt Bacterial Infection
    L-Valine-1- 13C ((S)-Valine-1- 13C) is the 13C-labeled L-Valine (HY-N0717). L-Valine ((S)-Valine) is a nonlinear semiorganic material. L-Valine causes lipid peroxidation and accumulation of malondialdehyde (MDA), exhibits inhibitory activity against cyanobacteria. L-Valine inhibits multidrug-resistant bacteria through activation of PI3K/Akt signaling pathway and inhibition of arginase .
    L-Valine-1-13C
  • HY-146683
    KS106

    		Aldehyde Dehydrogenase (ALDH) Apoptosis Cancer
    KS106 is a potent ALDH inhibitor with IC50s of 334, 2137, 360 nM for ALDH1A1, ALDH2, and ALDH3A1, respectively. KS106 shows antiproliferative and anticancer effects with low low toxic.KS106 significantly increases ROS activity, lipid peroxidation and toxic aldehyde accumulation. KS106 induces apoptosis and cell cycle arrest at the G2/M phase .
    KS106
  • HY-139369
    QD394
    1 Publications Verification

    		 Reactive Oxygen Species (ROS) Cancer
    QD394 is a reactive oxygen species (ROS) inducer that can induce lipid peroxidation, increase intracellular ROS accumulation, inhibit STAT3 phosphorylation, and induce ferroptosis .
    QD394
  • HY-N0717S
    L-Valine-15N

    (S)-Valine-15N

    		 Isotope-Labeled Compounds Arginase Akt Bacterial Infection
    L-Valine- 15N ((S)-Valine- 15N) is the 15N-labeled L-Valine (HY-N0717). L-Valine ((S)-Valine) is a nonlinear semiorganic material. L-Valine causes lipid peroxidation and accumulation of malondialdehyde (MDA), exhibits inhibitory activity against cyanobacteria. L-Valine inhibits multidrug-resistant bacteria through activation of PI3K/Akt signaling pathway and inhibition of arginase .
    L-Valine-15N
  • HY-N0717S1
    L-Valine-13C5,15N

    (S)-Valine-13C5,15N

    		 Isotope-Labeled Compounds Arginase Akt Bacterial Infection
    L-Valine- 13C5, 15N ((S)-Valine- 13C5, 15) is the 13C- and 15N-labeled L-Valine (HY-N0717). L-Valine ((S)-Valine) is a nonlinear semiorganic material. L-Valine causes lipid peroxidation and accumulation of malondialdehyde (MDA), exhibits inhibitory activity against cyanobacteria. L-Valine inhibits multidrug-resistant bacteria through activation of PI3K/Akt signaling pathway and inhibition of arginase .
    L-Valine-13C5,15N
  • HY-163654
    Ferroptosis-IN-8

    		Ferroptosis Cancer
    Ferroptosis-IN-8 is a potent ferroptosis inhibitor with an EC50 of 40.49 nM. Ferroptosis-IN-8 effectively reduces lipid ROS levels in cells. Ferroptosis-IN-8 act as an antioxidant by capturing lipid radicals, leading to a reduction in the accumulation of harmful lipid peroxides and, ultimately, inhibiting ferroptosis .
    Ferroptosis-IN-8
  • HY-W009300
    4-Hydroxyestrone
    1 Publications Verification

    4-OHE1

    		 Endogenous Metabolite Estrogen Receptor/ERR Sirtuin MDM-2/p53 PDI Ferroptosis Reactive Oxygen Species (ROS) Neurological Disease Metabolic Disease Cancer
    4-Hydroxyestrone (4-OHE1) is a brain-penetrant estrogen metabolite. 4-Hydroxyestrone shows neuroprotective effects involving increased cytoplasmic localization of p53 resulting from SIRT1-mediated p53 deacetylation. 4-Hydroxyestrone relies on PDI to mediate its protective effect against chemically induced ferroptosis in estrogen receptor-negative cancer cells. 4-Hydroxyestrone inhibits lipid peroxidation and lipid-ROS accumulation. 4-Hydroxyestrone blocks preovulatory luteinizing hormone surges in Rattus norvegicus. 4-Hydroxyestrone can be used for the researches of neurodegeneration, breast cancer and endocrine disease .
    4-Hydroxyestrone
  • HY-178364
    GPX4-IN-19

    		Glutathione Peroxidase Ferroptosis Lipoxygenase Reactive Oxygen Species (ROS) DNA/RNA Synthesis Cancer
    GPX4-IN-19 is an effective GPX4 inhibitor (IC50 = 0.311 μM), covalently binds to the Sec 46 site of GPX4. GPX4-IN-19 shows strong anti-proliferative activity with high ferroptosis selectivity. GPX4-IN-19 causes intracellular Fe 2+ accumulation, leading to increased levels of lipid peroxides (LPOs) and reactive oxygen species (ROS), which induces ferroptosis and subsequently results in DNA damage. GPX4-IN-19 can be used for the study of Triple-Negative Breast Cancer (TNBC) .
    GPX4-IN-19
  • HY-N3027
    Soyasaponin Aa
    1 Publications Verification

    		 PPAR Reactive Oxygen Species (ROS) Metabolic Disease
    Soyasaponin Aa is a soyasaponin that can be found in soy. Soyasaponin Aa suppresses PPARγ transcriptional activity, reduces PPARγ and C/EBPα expression, inhibits adipocyte differentiation and lipid accumulation, and reduces adipogenic marker gene expression. Soyasaponin Aa reduces hydrogen peroxide-induced reactive oxygen species (ROS) production and malondialdehyde levels. Soyasaponin Aa exhibits cellular antioxidant activity. Soyasaponin Aa can be used for the research of obesity .
    Soyasaponin Aa
  • HY-179041
    SZ0232

    		PGE synthase Prostaglandin Receptor MDM-2/p53 Amino acid Transporter Glutathione Peroxidase Ferroptosis Metabolic Disease Endocrinology
    SZ0232 is a selective mPGES-2 inhibitor. SZ0232 binds to the active site of mPGES-2 via hydrogen bonds and π-π stacking, reduces the production of prostaglandin E2 (PGE2) and blocks the PGE2-EP3 pathway. SZ0232 regulates Ferroptosis by activating the heme-dependent p53/SLC7A11/GPX4 axis, inhibits lipid peroxidation, and protects renal tubules. SZ0232 enhances glucose-stimulated insulin secretion, inhibits β-cell senescence, and improves glucose homeostasis. SZ0232 reduces renal lipid accumulation, alleviates fibrosis, and ameliorates renal dysfunction in diabetic mice. SZ0232 inhibits renal cyst growth in polycystic kidney disease models. SZ0232 exhibits an insulinotropic effect that strengthens with the increase of animal age. SZ0232 can be used in studies related to type 2 diabetes, acute kidney injury, diabetic kidney disease, and autosomal dominant polycystic kidney disease .
    SZ0232
  • HY-113402R
    Gamma-glutamylcysteine (Standard)

    γ-Glu-Cys (Standard)

    		 Reference Standards Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Inflammation/Immunology
    Gamma-glutamylcysteine (Standard) is the analytical standard of Gamma-glutamylcysteine. This product is intended for research and analytical applications. Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.
    Gamma-glutamylcysteine (Standard)
  • HY-34765
    Propiolamide

    		Glutathione Peroxidase Reactive Oxygen Species (ROS) Ferroptosis Apoptosis Cancer
    Propiolamide is a monooxygenase (MMO) system activator and glutathione peroxidase 4 (GPX4) inhibitor. Propiolamide induces ROS production through interaction with the MMO system. Propiolamide promotes the accumulation of intracellular cytotoxic lipid peroxides and induces ferroptosis. Propiolamide induces programmed cell death via the apoptosis pathway. Propiolamide can be used in cancer research .
    Propiolamide
  • HY-170509
    Ferroptosis-IN-17

    		Ferroptosis Glutathione Peroxidase Cardiovascular Disease Neurological Disease Cancer
    Ferroptosis-IN-17 (Compound 18) is a ferroptosis (Ferroptosis) inhibitor with an EC50 value of 0.57 μM. Ferroptosis-IN-17 reduces intracellular ferrous ion accumulation, lipid peroxidation, and effectively restores the levels of glutathione (GSH) and glutathione peroxidase 4 (GPX4). Ferroptosis-IN-17 shows good solubility and significant metabolic stability in rat plasma. Ferroptosis-IN-17 is promising for research in tumor suppression, neurodegenerative diseases, and cardiovascular diseases .
    Ferroptosis-IN-17
  • HY-173119
    SKLB-D18

    		ERK Autophagy Apoptosis p62 mTOR Reactive Oxygen Species (ROS) Ferroptosis Cancer
    SKLB-D18 is an orally active ERK1/2/ERK5 inhibitor, with an IC50 of 38.69 nM and a Kd of 126.9 nM against human ERK1, an IC50 of 40.12 nM and a Kd of 209.8 nM against ERK2, and an IC50 of 59.72 nM and a Kd 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 .
    SKLB-D18
  • HY-172896
    FSP1-IN-1

    		Ferroptosis Cancer
    FSP1-IN-1 (compound 39) is a potent FSP1 inhibitor with an IC50 of 35 nM. FSP1-IN-1 enhances RSL3 (HY-100218A)-induced lipid peroxide accumulation and sensitizes cancer cells to ferroptosis .
    FSP1-IN-1
  • HY-162106
    PROTAC GPX4 degrader-2

    		Ferroptosis PROTACs Glutathione Peroxidase Cancer
    PROTAC GPX4 degrader-2 (compound 18a) is a proteolysis targeting chimeras (PROTACs) that can degrade glutathione peroxidase 4 (GPX4), with the DC50, 48h value of 1.68 μM. PROTAC GPX4 degrader-2 induces the accumulation of lipid peroxides and mitochondrial depolarization, subsequently triggering ferroptosis. PROTAC GPX4 degrader-2 has anti-proliferative effect .
    PROTAC GPX4 degrader-2
  • HY-174345
    Ferroptosis inducer-8

    		ACSL Family Ferroptosis Glutathione Peroxidase Reactive Oxygen Species (ROS) Cancer
    Ferroptosis inducer-8 is a ferroptosis inducer with high selectivity for other cell death mechanism. Ferroptosis inducer-8 induces ferroptosis by affecting ACSL4, GPX4, and FTH1, thereby disrupting intracellular iron homeostasis and the GSH/GPX4 antioxidant defense system, ultimately leading to the accumulation of lipid peroxidation. Ferroptosis inducer-8 also induces ROS production. Ferroptosis inducer-8 inhibits tumor growth and can be used for research of triple-negative breast cancer (TNBC) .
    Ferroptosis inducer-8
  • HY-P1723A
    Spexin TFA

    Neuropeptide Q TFA

    		 Neuropeptide Y Receptor Apoptosis Ferroptosis Autophagy Cardiovascular Disease Metabolic Disease
    Spexin (Neuropeptide Q) TFA is a selective agonist of galanin receptors GAL2 and GAL3, and is a conserved peptide that functions as a neurotransmitter/neuromodulator and endocrine factor. Spexin TFA can function through both central and peripheral actions. Spexin TFA upregulates Beclin 1 to inhibit ferroptosis induced by excessive autophagy, reduces the uptake of long-chain fatty acids by adipocytes, and regulates energy metabolism by increasing lipid oxidation (e.g., reducing the respiratory exchange ratio in rodents). Spexin TFA improves cardiac function in the Doxorubicin hydrochloride (HY-15142)-induced cardiotoxicity model, protects mitochondrial membrane potential, and reduces iron accumulation and lipid peroxidation. Spexin TFA can be used to study obesity and its related metabolic disorders, cardiovascular diseases (e.g., cardioprotection), and side effects of tumor chemotherapy .
    Spexin TFA
  • HY-179384
    PROTAC FSP1 degrader 1

    		ACSL Family PROTACs Ferroptosis Glutathione Peroxidase Transferrin Receptor Reactive Oxygen Species (ROS) Cancer
    PROTAC FSP1 degrader 1 is a highly efficient and selective PROTAC degrader targeting FSP1. PROTAC FSP1 degrader 1 significantly induces the accumulation of intracellular lipid peroxides. PROTAC FSP1 degrader 1 exhibits synergistic induction of ferroptosis with GPX4 inhibitors. PROTAC FSP1 degrader 1 can induce ROS production. PROTAC FSP1 degrader 1 upregulates the mRNA expression of ferroptosis-related proteins (GPX4, FTH1, ACSL4, TfR1, FSP1). PROTAC FSP1 degrader 1 can be used for the study of triple-negative breast cancer .
    PROTAC FSP1 degrader 1
  • HY-N0468R
    Rebaudioside D (Standard)

    		Reference Standards Acetyl-CoA Carboxylase FXR Metabolic Disease
    Rebaudioside D (Standard) is the analytical standard of Rebaudioside D. This product is intended for research and analytical applications. Rebaudioside D is an orally active sweetener that targets and activates FXR, modulates Acetyl-CoA Carboxylase, and inhibits 3-hydroxy-3-methylglutaryl-CoA reductase. Rebaudioside D regulates bile acid homeostasis and lipid metabolism, reduces the synthesis rates of fatty acids and cholesterol, and exerts multiple effects including anti-adipogenesis, hepatoprotection, anti-steatosis, gut microbiota modulation, enhancement of secondary bile acid metabolism, anti-endotoxin activity, regulation of bile acid transport, and inhibition of bile acid efflux. Rebaudioside D also reduces body weight gain, visceral fat accumulation, hepatic triglyceride and cholesterol accumulation, hepatic lipid peroxidation, and decreases the circulating level of lipopolysaccharide-binding protein. Rebaudioside D additionally enhances the secondary bile acid metabolic pathway of intestinal bacteria, upregulates the gene expression of ileal organic solute transporter α, and downregulates the gene expression of hepatic bile salt export pump. Rebaudioside D does not affect glucose homeostasis, alter total caloric intake or fecal energy excretion, induce weight gain, exacerbate obesity, promote hepatic steatosis, impair brown adipose tissue function, nor change skeletal muscle metabolism-related proteins. Rebaudioside D can be used in diet-induced obesity and obesity-related research .
    Rebaudioside D (Standard)
  • HY-N6929R
    Angelic acid (Standard)

    		Reference Standards Ferroptosis Keap1-Nrf2 Reactive Oxygen Species (ROS) Neurological Disease Cancer
    Angelic acid (Standard)) is the analytical standard of Angelic acid (HY-N6929). This product is intended for research and analytical applications. Angelic acid is a ferroptosis inducer, targeting NRF2 degradation. Angelic acid binds to NRF2 protein and promotes NRF2 degradation via ubiquitination-proteasome pathway, relieves the inhibitory effect of NRF2 on oxidative stress and lipid peroxidation. Then, Angelic acid induces ferroptosis in tumor cells. Angelic acid can enhance the accumulation of intracellular reactive oxygen species (ROS), upregulate ferroptosis-related markers CHAC1 and PTGS2, and synergize with ferroptosis inducers to enhance anti-tumor effects. Angelic acid also has the activity of scavenging UVA-induced ROS in vitro, inhibiting skin fibroblast senescence and extracellular matrix degradation. Angelic Acid helps wound healing with sedative activity .
    Angelic acid (Standard)
  • HY-113402AR
    Gamma-glutamylcysteine TFA (Standard)

    γ-Glu-Cys TFA (Standard)

    		 Interleukin Related TNF Receptor Endogenous Metabolite Reference Standards AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine (TFA) (Standard) is the analytical standard of Gamma-glutamylcysteine (TFA). This product is intended for research and analytical applications. Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.
    Gamma-glutamylcysteine TFA (Standard)
  • HY-170959
    NYY-6a

    		Ferroptosis Neurological Disease Metabolic Disease
    NYY-6a is a Ferroptosis inhibitor. NYY-6a shows significant inhibitory activity against RSL3-induced ferroptosis across 786-O and HT-1080 cells with EC50s of 52 and 50 nM, respectively. NYY-6a functions as a radical trapping antioxidant (RTA) with efficacy of diminishing lipid peroxidation comparable to ferrostatin-1 and liproxtatin-1. NYY-6a is potential for ferroptosis related pathologies reasearch .
    NYY-6a
  • HY-168042
    Antibacterial agent 243

    		Bacterial Fungal Infection
    Antibacterial agent 243 is an antibacterial agent, with EC50 values of 0.64 mg/L for Valsa mali, 26 mg/L for allicin, and 0.33 mg/L for tebuconazole. Antibacterial agent 243 can induce hyphal shrinkage and collapse, trigger the accumulation of reactive oxygen species inside cells, regulate antioxidant enzyme activity, initiate lipid peroxidation, and ultimately cause irreversible oxidative damage to Valsa mali cells .
    Antibacterial agent 243
  • HY-161388
    NSCLC-IN-1

    		Ferroptosis Mitophagy Cancer
    NSCLC-IN-1 (Compound A10-2) induces mitophagy and ferroptosis through targeting transmembrane BAX inhibitor motif containing 6 (TMBIM6). NSCLC-IN-1 induces mitochondrial Ca 2+ imbalance, leading to mitochondrial damage. NSCLC-IN-1 reduces intracellular glutathione (GSH), increases the accumulation of lipid peroxides (LPO) and malondialdehyde (MDA) content. NSCLC-IN-1 is a potent anti-NSCLC agent .
    NSCLC-IN-1
  • HY-178305S
    L-Valine-d

    		Isotope-Labeled Compounds Bacterial Arginase Akt Infection
    L-Valine-d is the deuterium labeled L-Valine (HY-N0717). L-Valine ((S)-Valine) is a nonlinear semiorganic material. L-Valine causes lipid peroxidation and accumulation of malondialdehyde (MDA), exhibits inhibitory activity against cyanobacteria. L-Valine inhibits multidrug-resistant bacteria through activation of PI3K/Akt signaling pathway and inhibition of arginase .
    L-Valine-d
  • HY-N0717S8
    L-Valine-d1

    (S)-Valine-d1

    		 Isotope-Labeled Compounds Arginase Akt Bacterial Infection
    L-Valine-d1 ((S)-Valine-d1) is the deuterium labeled L-Valine (HY-N0717). L-Valine ((S)-Valine) is a nonlinear semiorganic material. L-Valine causes lipid peroxidation and accumulation of malondialdehyde (MDA), exhibits inhibitory activity against cyanobacteria. L-Valine inhibits multidrug-resistant bacteria through activation of PI3K/Akt signaling pathway and inhibition of arginase .
    L-Valine-d1
  • HY-N0717S5
    L-Valine-2-13C

    (S)-Valine-13C

    		 Isotope-Labeled Compounds Arginase Akt Bacterial Infection
    L-Valine-2- 13C ((S)-Valine-2- 13C) is the 13C-labeled L-Valine (HY-N0717). L-Valine ((S)-Valine) is a nonlinear semiorganic material. L-Valine causes lipid peroxidation and accumulation of malondialdehyde (MDA), exhibits inhibitory activity against cyanobacteria. L-Valine inhibits multidrug-resistant bacteria through activation of PI3K/Akt signaling pathway and inhibition of arginase .
    L-Valine-2-13C
  • HY-N3027R
    Soyasaponin Aa (Standard)

    		Reference Standards PPAR Reactive Oxygen Species (ROS) Metabolic Disease
    Soyasaponin Aa (Standard) is the analytical standard of Soyasaponin Aa (HY-N3027). Soyasaponin Aa is a soyasaponin that can be found in soy. Soyasaponin Aa suppresses PPARγ transcriptional activity, reduces PPARγ and C/EBPα expression, inhibits adipocyte differentiation and lipid accumulation, and reduces adipogenic marker gene expression. Soyasaponin Aa reduces hydrogen peroxide-induced reactive oxygen species (ROS) production and malondialdehyde levels. Soyasaponin Aa exhibits cellular antioxidant activity. Soyasaponin Aa can be used for the research of obesity .
    Soyasaponin Aa (Standard)
  • HY-N0717S9
    L-Valine-15N,d8

    (S)-Valine-15N,d8

    		 Isotope-Labeled Compounds Arginase Akt Bacterial Infection
    L-Valine- 15N,d8 ((S)-Valine- 15N,d8) is the deuterium and 15N labeled L-Valine (HY-N0717). L-Valine ((S)-Valine) is a nonlinear semiorganic material. L-Valine causes lipid peroxidation and accumulation of malondialdehyde (MDA), exhibits inhibitory activity against cyanobacteria. L-Valine inhibits multidrug-resistant bacteria through activation of PI3K/Akt signaling pathway and inhibition of arginase .
    L-Valine-15N,d8
  • HY-172092
    BG11

    		Apoptosis Ferroptosis Cancer
    BG11 induces the accumulation of Fe 2+ and intracellular lipid peroxides, induces ferroptosis. BG11 regulates the expression of Bax and Bcl-2 proteins, and induces apoptosis in MDA-MB-231 cell. BG11 arrests the cell cycle at G0/G1 and S phase, inhibits the proliferation of TNBC cancer cell (IC50 for MDA-MB-231 and BT549 is 0.49 μM and 0.52 μM), and inhibits the cell migration and invasion. BG11 exhibits antitumor efficacy in mouse models .
    BG11
  • HY-N0717S7
    L-Valine-1-13C,15N

    (S)-Valine-1-13C,15N

    		 Isotope-Labeled Compounds Arginase Akt Bacterial Infection
    L-Valine-1- 13C, 15N ((S)-Valine-1- 13C, 15N) is the 13C- and 15N-labeled L-Valine (HY-N0717). L-Valine ((S)-Valine) is a nonlinear semiorganic material. L-Valine causes lipid peroxidation and accumulation of malondialdehyde (MDA), exhibits inhibitory activity against cyanobacteria. L-Valine inhibits multidrug-resistant bacteria through activation of PI3K/Akt signaling pathway and inhibition of arginase .
    L-Valine-1-13C,15N
  • HY-W009300S
    4-Hydroxyestrone-d4

    4-OHE1-d4

    		 Endogenous Metabolite Isotope-Labeled Compounds Estrogen Receptor/ERR Sirtuin MDM-2/p53 PDI Ferroptosis Reactive Oxygen Species (ROS) Neurological Disease Metabolic Disease Cancer
    4-Hydroxyestrone (4-OHE1)-d4 is the deuterium labeled 4-Hydroxyestrone (HY-W009300). 4-Hydroxyestrone is a brain-penetrant estrogen metabolite. 4-Hydroxyestrone shows neuroprotective effects involving increased cytoplasmic localization of p53 resulting from SIRT1-mediated p53 deacetylation. 4-Hydroxyestrone relies on PDI to mediate its protective effect against chemically induced ferroptosis in estrogen receptor-negative cancer cells. 4-Hydroxyestrone inhibits lipid peroxidation and lipid-ROS accumulation. 4-Hydroxyestrone blocks preovulatory luteinizing hormone surges in Rattus norvegicus. 4-Hydroxyestrone can be used for the researches of neurodegeneration, breast cancer and endocrine disease .
    4-Hydroxyestrone-d4
  • HY-W009300S1
    4-Hydroxyestrone-13C6

    4-OHE1-13C6

    		 Isotope-Labeled Compounds Endogenous Metabolite Estrogen Receptor/ERR Sirtuin MDM-2/p53 PDI Ferroptosis Reactive Oxygen Species (ROS) Neurological Disease Metabolic Disease Cancer
    4-Hydroxyestrone (4-OHE1)- 13C6 is a 13C-labeled 4-Hydroxyestrone (HY-W009300). 4-Hydroxyestrone is a brain-penetrant estrogen metabolite. 4-Hydroxyestrone shows neuroprotective effects involving increased cytoplasmic localization of p53 resulting from SIRT1-mediated p53 deacetylation. 4-Hydroxyestrone relies on PDI to mediate its protective effect against chemically induced ferroptosis in estrogen receptor-negative cancer cells. 4-Hydroxyestrone inhibits lipid peroxidation and lipid-ROS accumulation. 4-Hydroxyestrone blocks preovulatory luteinizing hormone surges in Rattus norvegicus. 4-Hydroxyestrone can be used for the researches of neurodegeneration, breast cancer and endocrine disease .
    4-Hydroxyestrone-13C6
  • HY-N0717S3
    L-Valine-13C5,15N,d2

    (S)-Valine-13C5,15N,d2

    		 Isotope-Labeled Compounds Arginase Akt Bacterial Infection
    L-Valine- 13C5, 15N,d2 ((S)-Valine- 13C5, 15N,d2) is the deuterium, 13C-, and 15N-labeled L-Valine (HY-N0717). L-Valine ((S)-Valine) is a nonlinear semiorganic material. L-Valine causes lipid peroxidation and accumulation of malondialdehyde (MDA), exhibits inhibitory activity against cyanobacteria. L-Valine inhibits multidrug-resistant bacteria through activation of PI3K/Akt signaling pathway and inhibition of arginase .
    L-Valine-13C5,15N,d2
  • HY-N0717S2
    L-Valine-13C5,15N,d8

    (S)-Valine-13C5,15N,d8

    		 Isotope-Labeled Compounds Arginase Akt Bacterial Infection
    L-Valine- 13C5, 15N,d8 ((S)-Valine- 13C5, 15N,d8) is the deuterium, 13C-, and 15N-labeled L-Valine (HY-N0717). L-Valine ((S)-Valine) is a nonlinear semiorganic material. L-Valine causes lipid peroxidation and accumulation of malondialdehyde (MDA), exhibits inhibitory activity against cyanobacteria. L-Valine inhibits multidrug-resistant bacteria through activation of PI3K/Akt signaling pathway and inhibition of arginase .
    L-Valine-13C5,15N,d8
  • HY-113402B
    Gamma-glutamylcysteine ammonium

    γ-Glu-Cys ammonium

    		 Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine ammonium (γ-Glu-Cys ammonium) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine ammonium activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine ammonium regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine ammonium is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
    Gamma-glutamylcysteine ammonium

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