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Pathways Recommended: MAPK/ERK Pathway
Results for "

lysosomal pathway

" in MedChemExpress (MCE) Product Catalog:

56

Inhibitors & Agonists

1

Screening Libraries

1

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2

Peptides

1

Inhibitory Antibodies

16

Natural
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8

Isotope-Labeled Compounds

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-N2334
    Glycochenodeoxycholic acid
    5 Publications Verification

    Chenodeoxycholylglycine

    		 Endogenous Metabolite Apoptosis STAT BCL6 Interleukin Related Caspase Metabolic Disease Cancer
    Glycochenodeoxycholic acid (Chenodeoxycholylglycine) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC) .
    Glycochenodeoxycholic acid
  • HY-N2334A
    Glycochenodeoxycholic acid sodium salt
    5 Publications Verification

    Chenodeoxycholylglycine sodium salt; Sodium glycochenodeoxycholate

    		 Endogenous Metabolite Apoptosis STAT BCL6 Interleukin Related Caspase Metabolic Disease Cancer
    Glycochenodeoxycholic acid sodium salt (Sodium glycochenodeoxycholate) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid sodium salt inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid sodium salt induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid sodium salt is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC) .
    Glycochenodeoxycholic acid sodium salt
  • HY-13817
    IU1
    Maximum Cited Publications
    25 Publications Verification

    		 Deubiquitinase Autophagy Apoptosis 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 .
    IU1
  • HY-33878
    2-PPA

    		Potassium Channel Proton Pump Neurological Disease
    2-PPA is a lysosomal potassium and proton channel TMEM175 pore blocker. 2-PPA binds at a TMEM175 pore site to occlude potassium and proton ion permeation pathways. 2-PPA increases lysosomal macromolecule catabolism, accelerates macropinocytosis. 2-PPA binds to hepatic protein in covalent. 2-PPA can be used for the research of Parkinson's disease .
    2-PPA
  • HY-N1163
    Tetrahydroalstonine

    (-)-Tetrahydroalstonine

    		 Adrenergic Receptor Atg8/LC3 Akt mTOR Neurological Disease Endocrinology
    Tetrahydroalstonine ((-)-Tetrahydroalstonine) is an indole alkaloid and a selective α₂-adrenergic receptor antagonist. Tetrahydroalstonine exhibits certain neuroprotective effects. Tetrahydroalstonine can regulate autophagy-lysosomal function by activating the Akt/mTOR pathway, significantly reducing OGD/R-induced primary cortical neuronal injury .
    Tetrahydroalstonine
  • HY-155747
    FDW028
    1 Publications Verification

    		 Autophagy Akt mTOR Cancer
    FDW028 a potent and highly selective FUT8 inhibitor. FUT8 exhibits potent anti-tumor activity by defucosylation and impelling lysosomal degradation of B7-H3 through the chaperone-mediated autophagy (CMA) pathway. FDW028 can be used for metastatic colorectal cancer (mCRC) research .
    FDW028
  • HY-107811
    Harmol
    1 Publications Verification

    		 Autophagy α-synuclein Apoptosis Monoamine Oxidase Mitosis Neurological Disease Cancer
    Harmol is an orally active β-carboline alkaloid. Harmol is a TFEB activator and monoamine oxidase inhibitor. Harmol can induce cell mitosis, Autophagy and Apoptosis. Harmol promotes the degradation of α-synuclein by regulating the autophagy-lysosomal pathway. Harmol has anti-tumor, anti-depressant and anti-aging activities. Harmol improves motor impairment in a mouse Parkinson's disease model .
    Harmol
  • HY-148118A
    Tri-GalNAc(OAc)3 TFA

    		LYTACs Cancer
    Tri-GalNAc(OAc)3 TFA is a trivalent N-acetylgalactosamine (GalNAc) derivative that can be used to synthesize GalNAc-LYTAC. Tri-GalNAc is a specific ligand targeting the asialoglycoprotein receptor (ASGPR), mediating the endocytosis and transport of cell surface proteins (such as EGFR, HER2) to lysosomes for degradation by lysosomal targeting chimeras (LYTACs). Tri-GalNAc significantly reduces the level of target proteins and inhibits downstream signaling pathways (such as EGFR-mediated Akt and MAPK signals). Tri-GalNAc(OAc)3 TFA can be used for hepatocyte targeting studies, and can degrade carcinogenic membrane proteins and inhibit tumor cell proliferation in liver cancer cell models .
    Tri-GalNAc(OAc)3 TFA
  • HY-N0059
    D-Arabinose

    		Parasite Bacterial AMPK PPAR Infection Neurological Disease Metabolic Disease
    D-Arabinose is is an orally active antidepressant and a growth inhibitor of C. elegans (IC50 is 7.5 mM). D-Arabinose can penetrate the blood-brain barrier, selectively interfere with the metabolism of D-ribose and D-fructose, and inhibit the growth of nematodes. D-Arabinose can also inhibit the synthesis of cell biofilm and exert antibacterial activity. D-Arabinose activates the ACSS2-PPARγ/TFEB-CRTC1 axis through the lysosomal AXIN-LKB1-AMPK pathway, inducing CRTC1 transcription, exerts antidepressant-like activity. D-Arabinose is the ring-opened form of the aldopentose D-?Arabinose (HY-N7082) .
    D-Arabinose
  • HY-W046353
    2-Methoxycinnamaldehyde

    o-Methoxycinnamaldehyde

    		 Apoptosis NF-κB Topoisomerase Mitochondrial Metabolism Caspase Cancer
    2-Methoxycinnamaldehyde (o-Methoxycinnamaldehyde) is a natural compound that can be isolated from Cinnamomum cassia. 2-Methoxycinnamaldehyde inhibits topoisomerase-I/II and NF-κB signaling pathway, causes mitochondrial dysfunction, induces lysosomal vesiculation, thereby leading to DNA damage and cell apoptosis. 2-Methoxycinnamaldehyde exhibits antitumor effects .
    2-Methoxycinnamaldehyde
  • HY-N1983
    Caudatin
    1 Publications Verification

    		 Apoptosis Autophagy Reactive Oxygen Species (ROS) Mitochondrial Metabolism PARP Caspase Bcl-2 Family VEGFR FAK WDR5 p38 MAPK JNK PPAR Neurological Disease Inflammation/Immunology Cancer
    Caudatin is an orally active and brain-penetrant C-21 steroidal found in Cynanchum bungei decne with a variety of biological activities. Caudatin can inhibit cell proliferation, migration, invasion, cause cell phase arrest, induce apoptosis, autophagy, ROS prodution and loss of mitochondrial membrane potential. Caudatin activates PARP, caspase-3, -7, -9, upregulates pro-apoptotic Bad and Bax and downregulates anti-apoptotic Bcl-2 and Bcl-XL. Caudatin suppresses VEGF, FAK phosphorylation, upregulates p21, p27, DR5 protein expression, activates the p38 MAPK, JNK and PPARα/TFEB-mediated autophagy-lysosomal signaling pathways. Caudatin can be used for the research of cancer, inflammation and neurological disease, such as glioma and Alzheimer's disease .
    Caudatin
  • HY-N7082
    D-Arabinopyranose

    		Parasite Bacterial AMPK PPAR Infection Neurological Disease Metabolic Disease
    D-Arabinopyranose is a rare aldehyde pentose, and its ring-opened form is D-arabinose (HY-N0059). D-arabinose is is an orally active antidepressant and a growth inhibitor of C. elegans (IC50 is 7.5 mM). D-arabinose can penetrate the blood-brain barrier, selectively interfere with the metabolism of D-ribose and D-fructose, and inhibit the growth of nematodes. D-arabinose can also inhibit the synthesis of cell biofilm and exert antibacterial activity. D-arabinose activates the ACSS2-PPARγ/TFEB-CRTC1 axis through the lysosomal AXIN-LKB1-AMPK pathway, inducing CRTC1 transcription, exerts antidepressant-like activity. D-arabinose is the ring-opened form of the aldopentose D-?Arabinose (HY-N7082) .
    D-Arabinopyranose
  • HY-125168
    EGA
    2 Publications Verification

    		 EGFR Infection Inflammation/Immunology
    EGA is an inhibitor that selectively targets the endosomal trafficking pathways. EGA targets the proteins involved in the endosomal trafficking pathways through which multiple toxins and viruses enter cells. EGA exerts its activity by inhibiting the trafficking from early endosomes to late endosomes, blocking the entry of multiple acid-dependent bacterial toxins and viruses into mammalian cells and delaying the lysosomal targeting and degradation of EGFR .
    EGA
  • HY-N0910
    Notoginsenoside Ft1
    1 Publications Verification

    		 PI3K mTOR Akt Apoptosis p38 MAPK ERK Transmembrane Glycoprotein Glutathione Reductase (GR) Estrogen Receptor/ERR Calcium Channel Ferroptosis G protein-coupled Bile Acid Receptor 1 FXR Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Notoginsenoside Ft1 is an orally active bioactive saponin. Notoginsenoside Ft1 inhibits the PI3K/AKT/mTOR signaling pathway, activates the p38 MAPK and ERK1/2 signaling pathways, and increases the proportion of CD8 + T cells, thereby inducing apoptosis and lysosomal cell death in various cancer cells, and promoting angiogenesis. Notoginsenoside Ft1 causes vasodilation by activating glucocorticoid receptors (GR) and estrogen receptor beta (ERβ) in endothelial cells. Notoginsenoside Ft1 increases intracellular Ca 2+ accumulation, reduces cAMP levels by activating a signaling network mediated through P2Y12 receptors, and promotes platelet aggregation, thereby exerting a procoagulant effect. Notoginsenoside Ft1 inhibits ferroptosis (ferroptosis) in renal tubular epithelial cells by activating the TGR5 receptor, thereby demonstrating a renal protective effect. Notoginsenoside Ft1 acts as a TGR5 agonist and an FXR antagonist to combat obesity and insulin resistance .
    Notoginsenoside Ft1
  • HY-170035
    GlcCer (d18:1/18:0)

    C18 Glucosyl(β) ceramide (d18:1/18:0); D-glucosyl-β-1,1' N-stearoyl-D-erythro-sphingosine

    		 Fungal Wnt β-catenin Infection Neurological Disease Cancer
    GlcCer (d18:1/18:0) (C18 Glucosyl(β) ceramide (d18:1/18:0)) is a glycosphingolipids that activates the Wnt/β-catenin pathway by targeting LRP6. GlcCer (d18:1/18:0) drives EMT, migration, invasion and GBA1-mediated liver cancer metastasis. GlcCer (d18:1/18:0) accumulates to impair lysosomal function and induce toxic α-synuclein aggregation. GlcCer (d18:1/18:0) supports growth, sporulation, germination and virulence in Penicillium digitatum. GlcCer (d18:1/18:0) is reduced in demyelinated mouse corpus callosum. GlcCer (d18:1/18:0) can be used for the research of liver cancer, synucleinopathies, fungal, Parkinson’s disease and Gaucher disease .
    GlcCer (d18:1/18:0)
  • HY-42709
    Z-Val-Ala-OH

    Carbobenzoxy-L-valyl-L-alanine

    		 Amino Acid Derivatives Cancer
    Z-Val-Ala-OH is a dipeptide derivative of valine and alanine. Z-Val-Ala-OH undergoes cleavage by cathepsin B and other lysosomal proteases to enable payload release following lysosomal internalization. Z-Val-Ala-OH can be used for the research of antibody-drug conjugate (ADC) development[1] .
    Z-Val-Ala-OH
  • HY-153880
    KRAS degrader-1

    		LYTACs Ras Cancer
    KRAS degrader-1 is a potent KRAS degrader. KRAS degrader-1 targets specific proteins for degradation via the autophagy-lysosomal degradation pathway. KRAS degrader-1 is suitable for use in cancer research. (Blue: KRAS G12C-IN-72 (HY-128414); Black: Linker (HY-175587); Pink: 5-Iodoindolin-2-one (HY-76986); Blue + Black: KRAS ligand-Linker Conjugate 7 (HY-175586)) .
    KRAS degrader-1
  • HY-N2334R
    Glycochenodeoxycholic acid (Standard)

    Chenodeoxycholylglycine (Standard)

    		 Reference Standards Endogenous Metabolite Apoptosis STAT BCL6 Interleukin Related Caspase Metabolic Disease Cancer
    Glycochenodeoxycholic acid (Standard) is the analytical standard of Glycochenodeoxycholic acid. This product is intended for research and analytical applications. Glycochenodeoxycholic acid (Chenodeoxycholylglycine) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC)[1][2][3][4].
    Glycochenodeoxycholic acid (Standard)
  • HY-N2334AR
    Glycochenodeoxycholic acid sodium salt (Standard)

    Chenodeoxycholylglycine sodium salt (Standard); Sodium glycochenodeoxycholate (Standard)

    		 Reference Standards Endogenous Metabolite Apoptosis STAT BCL6 Interleukin Related Caspase Metabolic Disease Cancer
    Glycochenodeoxycholic acid sodium salt (Standard) is the analytical standard of Glycochenodeoxycholic acid sodium salt. This product is intended for research and analytical applications. Glycochenodeoxycholic acid sodium salt (Sodium glycochenodeoxycholate) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid sodium salt inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid sodium salt induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid sodium salt is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC) .
    Glycochenodeoxycholic acid sodium salt (Standard)
  • HY-139973
    OAB-14

    		Amyloid-β Neurological Disease
    OAB-14, is a Bexarotene (HY-14171) derivative, improves Alzheimer's disease-related pathologies and cognitive impairments by increasing β-amyloid clearance in APP/PS1 mice. OAB-14 effectively ameliorates the dysfunction of the endosomal-autophagic-lysosomal pathway in APP/PS1 transgenic mice .
    OAB-14
  • HY-150286
    SM875

    		Prion Protein Neurological Disease
    SM875 is a cellular prion protein (PrP) degrader (IC50: 7.87 μM). SM875 targets PrP folding intermediates and promotes its degradation through the autophagy-lysosomal pathway. SM875 only acts on nascent, immature PrP molecules and has no effect on mature PrP before synthesis. SM875 can inhibit prion replication and has potential in the study of neurodegenerative diseases (i.e., prion diseases) .
    SM875
  • HY-N1983R
    Caudatin (Standard)

    		Reference Standards Apoptosis Autophagy Reactive Oxygen Species (ROS) Mitochondrial Metabolism PARP Caspase Bcl-2 Family VEGFR FAK WDR5 p38 MAPK JNK PPAR Neurological Disease Inflammation/Immunology Cancer
    Caudatin (Standard) is the analytical standard of Caudatin (HY-N1983). This product is intended for research and analytical applications. Caudatin is an orally active and brain-penetrant C-21 steroidal found in Cynanchum bungei decne with a variety of biological activities. Caudatin can inhibit cell proliferation, migration, invasion, cause cell phase arrest, induce apoptosis, autophagy, ROS prodution and loss of mitochondrial membrane potential. Caudatin activates PARP, caspase-3, -7, -9, upregulates pro-apoptotic Bad and Bax and downregulates anti-apoptotic Bcl-2 and Bcl-XL. Caudatin suppresses VEGF, FAK phosphorylation, upregulates p21, p27, DR5 protein expression, activates the p38 MAPK, JNK and PPARα/TFEB-mediated autophagy-lysosomal signaling pathways. Caudatin can be used for the research of cancer, inflammation and neurological disease, such as glioma and Alzheimer's disease .
    Caudatin (Standard)
  • HY-147656
    NAMPT degrader-1

    		ATTECs NAMPT Autophagy Cancer
    NAMPT degrader-1 (Compound A3), an autophagosome-tethering compound (ATTEC), is an nicotinamide phosphoribosyltransferase (NAMPT) degrader with an IC50 of 0.023 μM. NAMPT degrader-1 significantly induces the degradation of NAMPT through the autophagy-lysosomal pathway and shows excellent cellular antitumor potency .
    NAMPT degrader-1
  • HY-165550
    Sphingosine

    C22-D-erythro-Sphingosine

    		 Apoptosis Caspase Mitochondrial Metabolism Bcl-2 Family Metabolic Disease
    Sphingosine (C22-D-erythro-Sphingosine) is a metabolite of sphingolipid and a pro-Apoptotic signaling messenger. Sphingosine induces apoptosis via Caspase-dependent, mitochondria-dependent and lysosomal affinity detergent pathways, downregulates Bcl-2 and Bcl-xL, and truncates Bid and Bax. Sphingosine is used for cancer research .
    Sphingosine
  • HY-107811A
    Harmol hydrochloride

    		Autophagy α-synuclein Apoptosis Monoamine Oxidase Mitosis Neurological Disease Cancer
    Harmol hydrochloride is an orally active β-carboline alkaloid. Harmol hydrochloride is a TFEB activator and monoamine oxidase inhibitor. Harmol hydrochloride can induce cell mitosis, Autophagy and Apoptosis. Harmol hydrochloride promotes the degradation of α-synuclein by regulating the autophagy-lysosomal pathway. Harmol hydrochloride has anti-tumor, anti-depressant and anti-aging activities. Harmol hydrochloride improves motor impairment in a mouse Parkinson's disease model .
    Harmol hydrochloride
  • HY-113484
    Leukotriene B5

    LTB5

    		 Leukotriene Receptor Cancer
    Leukotriene B5 (LTB5) is a leukotriene with diverse biological activities. It is a metabolite of eicosapentaenoic acid formed through the 5-lipoxygenase (5-LO) pathway. LTB5 increases contraction of bullfrog lung strips ex vivo in a concentration-dependent manner. In vivo, LTB5 (100 nM) reduces tumor volume in mice injected with Tm1 murine melanoma cells. LTB5 also elicits chemokinesis and lysosomal enzyme release from polymorphonuclear leukocytes (PMNLs) 20- to 30-fold less, and induces platelet aggregation 8-fold less, potently than LTB4.
    Leukotriene B5
  • HY-162972
    PROTAC PD-L1 degrader-2

    		PROTACs PD-1/PD-L1 Cancer
    PROTAC PD-L1 degrader-2 (Compound 9i) is a PROTAC degrader for PD-L1, that inhibits PD-L1 with an IC50 of 197.4 nM and exhibits an affinity with PD-L1 with a Kd of 301 nM. PROTAC PD-L1 degrader-2 promotes the internalization of PD-L1 on the cell membrane, and induces PD-L1 degradation via the synergistic effect of the proteasome and lysosomal pathways. PROTAC PD-L1 degrader-2 can activate the immune system, and exhibits antitumor efficacy in MC38 C57BL/6 mouse model .
    PROTAC PD-L1 degrader-2
  • HY-N0059R
    D-Arabinose (Standard)

    		Reference Standards Parasite Bacterial AMPK PPAR Infection Neurological Disease Metabolic Disease
    D-Arabinose (Standard) is the analytical standard of D-Arabinose. This product is intended for research and analytical applications. D-Arabinose is is an orally active antidepressant and a growth inhibitor of C. elegans (IC50 is 7.5 mM). D-Arabinose can penetrate the blood-brain barrier, selectively interfere with the metabolism of D-ribose and D-fructose, and inhibit the growth of nematodes. D-Arabinose can also inhibit the synthesis of cell biofilm and exert antibacterial activity. D-Arabinose activates the ACSS2-PPARγ/TFEB-CRTC1 axis through the lysosomal AXIN-LKB1-AMPK pathway, inducing CRTC1 transcription, exerts antidepressant-like activity. D-Arabinose is the ring-opened form of the aldopentose D-?Arabinose (HY-N7082) .
    D-Arabinose (Standard)
  • HY-N0059S1
    D-Arabinose-13C-1

    		Isotope-Labeled Compounds Parasite Bacterial AMPK PPAR Infection Neurological Disease Metabolic Disease
    D-Arabinose- 13C-1 is the 13C labeled D-Arabinose (HY-N0059). D-Arabinose is is an orally active antidepressant and a growth inhibitor of C. elegans (IC50 is 7.5 mM). D-Arabinose can penetrate the blood-brain barrier, selectively interfere with the metabolism of D-ribose and D-fructose, and inhibit the growth of nematodes. D-Arabinose can also inhibit the synthesis of cell biofilm and exert antibacterial activity. D-Arabinose activates the ACSS2-PPARγ/TFEB-CRTC1 axis through the lysosomal AXIN-LKB1-AMPK pathway, inducing CRTC1 transcription, exerts antidepressant-like activity. D-Arabinose is the ring-opened form of the aldopentose D-?Arabinose (HY-N7082) .
    D-Arabinose-13C-1
  • HY-N0059S3
    D-Arabinose-13C-3

    		Isotope-Labeled Compounds Parasite Bacterial AMPK PPAR Infection Neurological Disease Metabolic Disease
    D-Arabinose- 13C-3 is the 13C labeled D-Arabinose (HY-N0059). D-Arabinose is is an orally active antidepressant and a growth inhibitor of C. elegans (IC50 is 7.5 mM). D-Arabinose can penetrate the blood-brain barrier, selectively interfere with the metabolism of D-ribose and D-fructose, and inhibit the growth of nematodes. D-Arabinose can also inhibit the synthesis of cell biofilm and exert antibacterial activity. D-Arabinose activates the ACSS2-PPARγ/TFEB-CRTC1 axis through the lysosomal AXIN-LKB1-AMPK pathway, inducing CRTC1 transcription, exerts antidepressant-like activity. D-Arabinose is the ring-opened form of the aldopentose D-?Arabinose (HY-N7082) .
    D-Arabinose-13C-3
  • HY-138813R
    N-Desethyl Sunitinib hydrochloride (Standard)

    SU-12662 hydrochloride (Standard)

    		 Reference Standards Drug Metabolite Cancer
    Glycochenodeoxycholic acid sodium salt (Standard) is the analytical standard of Glycochenodeoxycholic acid sodium salt. This product is intended for research and analytical applications. Glycochenodeoxycholic acid sodium salt (Sodium glycochenodeoxycholate) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid sodium salt inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid sodium salt induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid sodium salt is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC) .
    N-Desethyl Sunitinib hydrochloride (Standard)
  • HY-173150
    Hapalindole Q

    		YAP Cancer
    Hapalindole Q (Compound (+)-1) is an autophagy (Autophagy) inhibitor targeting YAP1. Hapalindole Q binds to the Hippo pathway transcription factor YAP1 with a Kd of 9.13 μM and induces its degradation via the chaperone-mediated autophagy (CMA) pathway. This process inhibits Rab7-mediated fusion of autophagosomes and lysosomes, thereby reducing overall autophagy levels without affecting lysosomal function. Hapalindole Q holds promise for research in cancer (e.g., liver cancer, breast cancer, etc.) .
    Hapalindole Q
  • HY-203817
    IITZ-02

    		Autophagy Apoptosis Mitochondrial Metabolism Cancer
    IITZ-02 is a lysosomotropic Autophagy inhibitor. IITZ-02 enhances autophagosome accumulation but inhibits autophagosomal degradation by impairing lysosomal function, finally inducing the inhibition of autophagy. IITZ-02 abolishes mitochondrial membrane potential and induces apoptosis through the mitochondria-mediated pathway. IITZ-02 has a potent antitumor activity in MDA-MB-231 xenograft mouse models. IITZ-02 can be used for cancers research .
    IITZ-02
  • HY-W046353R
    2-Methoxycinnamaldehyde (Standard)

    o-Methoxycinnamaldehyde (Standard)

    		 Reference Standards Apoptosis NF-κB Mitochondrial Metabolism Caspase Topoisomerase Cancer
    2-Methoxycinnamaldehyde (Standard) is the analytical standard of 2-Methoxycinnamaldehyde. This product is intended for research and analytical applications. 2-Methoxycinnamaldehyde (o-Methoxycinnamaldehyde) is a natural compound that can be isolated from Cinnamomum cassia. 2-Methoxycinnamaldehyde inhibits topoisomerase-I/II and NF-κB signaling pathway, causes mitochondrial dysfunction, induces lysosomal vesiculation, thereby leading to DNA damage and cell apoptosis. 2-Methoxycinnamaldehyde exhibits antitumor effects .
    2-Methoxycinnamaldehyde (Standard)
  • HY-107811R
    Harmol (Standard)

    		Apoptosis Monoamine Oxidase Autophagy α-synuclein Mitosis Reference Standards Neurological Disease Cancer
    Harmol (Standard) is the analytical standard of Harmol (HY-107811). This product is intended for research and analytical applications. Harmol hydrochloride is an orally active β-carboline alkaloid. Harmol hydrochloride is a TFEB activator and monoamine oxidase inhibitor. Harmol can induce cell mitosis, Autophagy and Apoptosis. Harmol promotes the degradation of α-synuclein by regulating the autophagy-lysosomal pathway. Harmol has anti-tumor, anti-depressant and anti-aging activities. Harmol improves motor impairment in a mouse Parkinson's disease model .
    Harmol (Standard)
  • HY-P10669
    NDI-Lyso

    		Caspase Apoptosis Cancer
    NDI-Lyso is a lysosome-targeted anticancer agent that induces the formation of rigid long fibers in cancer cell lysosomes through an enzyme-instructed self-assembly (EISA) mechanism catalyzed by cathepsin B. This process triggers lysosomal swelling, membrane permeabilization (LMP), and membrane disruption, ultimately leading to cancer cell apoptosis via a non-classical caspase-independent pathway. NDI-Lyso exhibits significant selective anticancer activity in various cancer cell lines and drug-resistant cancer cells (IC50 ~10 μM) while showing low toxicity to normal cells (IC50 > 60 μM) .
    NDI-Lyso
  • HY-175392
    PROTAC sEH-degrader-3

    		PROTACs Epoxide Hydrolase Metabolic Disease Inflammation/Immunology
    PROTAC sEH-degrader-3 (Compound 1a) is a targeted sEH PROTAC degrader that can selectively degrade sEH in the cytosol without affecting sEH in peroxisomes. PROTAC sEH-degrader-3 degrades sEH through a CRBN-dependent lysosomal pathway rather than the proteasome, with an IC50 of 0.8 nM against hsEH. PROTAC sEH-degrader-3 can inhibit endoplasmic reticulum stress and can be used in the research of inflammation, metabolic diseases, and other diseases related to endoplasmic reticulum stress. (Pink: sEH inhibitor (HY-114266); Black: Linker (HY-W008352); Blue: E3 Ligase Ligand (HY-14658)) .
    PROTAC sEH-degrader-3
  • HY-N0059S4
    D-Arabinose-d2

    		Isotope-Labeled Compounds Parasite Bacterial AMPK PPAR Infection Neurological Disease Metabolic Disease
    D-Arabinose-d2 is the deuterium labeled D-Arabinose (HY-N0059). D-Arabinose is is an orally active antidepressant and a growth inhibitor of C. elegans (IC50 is 7.5 mM). D-Arabinose can penetrate the blood-brain barrier, selectively interfere with the metabolism of D-ribose and D-fructose, and inhibit the growth of nematodes. D-Arabinose can also inhibit the synthesis of cell biofilm and exert antibacterial activity. D-Arabinose activates the ACSS2-PPARγ/TFEB-CRTC1 axis through the lysosomal AXIN-LKB1-AMPK pathway, inducing CRTC1 transcription, exerts antidepressant-like activity. D-Arabinose is the ring-opened form of the aldopentose D-?Arabinose (HY-N7082) .
    D-Arabinose-d2
  • HY-N0059S
    D-Arabinose-13C

    		Isotope-Labeled Compounds Parasite Bacterial AMPK PPAR Infection Neurological Disease Metabolic Disease
    D-Arabinose- 13C is the 13C labeled D-Arabinose (HY-N0059). D-Arabinose is is an orally active antidepressant and a growth inhibitor of C. elegans (IC50 is 7.5 mM). D-Arabinose can penetrate the blood-brain barrier, selectively interfere with the metabolism of D-ribose and D-fructose, and inhibit the growth of nematodes. D-Arabinose can also inhibit the synthesis of cell biofilm and exert antibacterial activity. D-Arabinose activates the ACSS2-PPARγ/TFEB-CRTC1 axis through the lysosomal AXIN-LKB1-AMPK pathway, inducing CRTC1 transcription, exerts antidepressant-like activity. D-Arabinose is the ring-opened form of the aldopentose D-?Arabinose (HY-N7082) .
    D-Arabinose-13C
  • HY-N0059S6
    D-Arabinose-d6

    		Isotope-Labeled Compounds Parasite Bacterial AMPK PPAR Infection Neurological Disease Metabolic Disease
    D-Arabinose-d6 is the deuterium labeled D-Arabinose (HY-N0059). D-Arabinose is is an orally active antidepressant and a growth inhibitor of C. elegans (IC50 is 7.5 mM). D-Arabinose can penetrate the blood-brain barrier, selectively interfere with the metabolism of D-ribose and D-fructose, and inhibit the growth of nematodes. D-Arabinose can also inhibit the synthesis of cell biofilm and exert antibacterial activity. D-Arabinose activates the ACSS2-PPARγ/TFEB-CRTC1 axis through the lysosomal AXIN-LKB1-AMPK pathway, inducing CRTC1 transcription, exerts antidepressant-like activity. D-Arabinose is the ring-opened form of the aldopentose D-?Arabinose (HY-N7082) .
    D-Arabinose-d6
  • HY-N0059S5
    D-Arabinose-d5

    		Isotope-Labeled Compounds Parasite Bacterial AMPK PPAR Infection Neurological Disease Metabolic Disease
    D-Arabinose-d5 is the deuterium labeled D-Arabinose (HY-N0059). D-Arabinose is is an orally active antidepressant and a growth inhibitor of C. elegans (IC50 is 7.5 mM). D-Arabinose can penetrate the blood-brain barrier, selectively interfere with the metabolism of D-ribose and D-fructose, and inhibit the growth of nematodes. D-Arabinose can also inhibit the synthesis of cell biofilm and exert antibacterial activity. D-Arabinose activates the ACSS2-PPARγ/TFEB-CRTC1 axis through the lysosomal AXIN-LKB1-AMPK pathway, inducing CRTC1 transcription, exerts antidepressant-like activity. D-Arabinose is the ring-opened form of the aldopentose D-?Arabinose (HY-N7082) .
    D-Arabinose-d5
  • HY-101349
    L 741742

    		Dopamine Receptor Apoptosis Autophagy PDGFR ERK mTOR Neurological Disease Cancer
    L 741742 is a highly selective and brain-penetrant D4 dopamine receptor antagonist, with Ki values of 3.5 nM, 770 nM and >1700 nM for human D4, D3 and D2 receptors, respectively. L 741742 suppresses PDGFRβ, ERK1/2, and mTOR signaling pathways, and impairs autophagic flux while disrupting lysosomal function.L 741742 induces G0/G1 cell-cycle arrest and apoptosis, promotes neuronal differentiation of normal human neural stem cells, selectively inhibits growth and clonogenic potential of glioblastoma neural stem cells and primary glioblastoma tumor cells, exerts synergistic effects with Temozolomide (TMZ) (HY-17364) against glioblastoma neural stem cells in vitro, and inhibits glioblastoma neural stem cell xenograft growth in immunocompromised mice. L 741742 can be used for the research of schizophrenia and glioblastoma .
    L 741742
  • HY-101349A
    L 741742 hydrochloride

    		Dopamine Receptor Apoptosis Autophagy PDGFR ERK mTOR Neurological Disease Cancer
    L 741742 hydrochloride is a highly selective and brain-penetrant D4 dopamine receptor antagonist, with Ki values of 3.5 nM, 770 nM and >1700 nM for human D4, D3 and D2 receptors, respectively. L 741742 hydrochloride suppresses PDGFRβ, ERK1/2, and mTOR signaling pathways, and impairs autophagic flux while disrupting lysosomal function.L 741742 hydrochloride induces G0/G1 cell-cycle arrest and apoptosis, promotes neuronal differentiation of normal human neural stem cells, selectively inhibits growth and clonogenic potential of glioblastoma neural stem cells and primary glioblastoma tumor cells, exerts synergistic effects with Temozolomide (TMZ) (HY-17364) against glioblastoma neural stem cells in vitro, and inhibits glioblastoma neural stem cell xenograft growth in immunocompromised mice. L 741742 hydrochloride can be used for the research of schizophrenia and glioblastoma .
    L 741742 hydrochloride
  • HY-N0059S2
    D-arabinose-13C-2

    		Isotope-Labeled Compounds Parasite Bacterial AMPK PPAR Infection Neurological Disease Metabolic Disease
    D-Arabinose- 13C-2 is the 13C labeled D-Arabinose (HY-N0059). D-Arabinose is is an orally active antidepressant and a growth inhibitor of C. elegans (IC50 is 7.5 mM). D-Arabinose can penetrate the blood-brain barrier, selectively interfere with the metabolism of D-ribose and D-fructose, and inhibit the growth of nematodes. D-Arabinose can also inhibit the synthesis of cell biofilm and exert antibacterial activity. D-Arabinose activates the ACSS2-PPARγ/TFEB-CRTC1 axis through the lysosomal AXIN-LKB1-AMPK pathway, inducing CRTC1 transcription, exerts antidepressant-like activity. D-Arabinose is the ring-opened form of the aldopentose D-?Arabinose (HY-N7082) .
    D-arabinose-13C-2
  • HY-N7082S
    D-Arabinopyranose-13C5

    		Isotope-Labeled Compounds Parasite Bacterial AMPK PPAR Infection Neurological Disease Metabolic Disease
    D-Arabinopyranos- 13C5 is 13C labeled D-Arabinopyranos (HY-N7082). D-Arabinopyranose is a rare aldehyde pentose, and its ring-opened form is D-arabinose (HY-N0059). D-arabinose is is an orally active antidepressant and a growth inhibitor of C. elegans (IC50 is 7.5 mM). D-arabinose can penetrate the blood-brain barrier, selectively interfere with the metabolism of D-ribose and D-fructose, and inhibit the growth of nematodes. D-arabinose can also inhibit the synthesis of cell biofilm and exert antibacterial activity. D-arabinose activates the ACSS2-PPARγ/TFEB-CRTC1 axis through the lysosomal AXIN-LKB1-AMPK pathway, inducing CRTC1 transcription, exerts antidepressant-like activity. D-arabinose is the ring-opened form of the aldopentose D-?Arabinose (HY-N7082) .
    D-Arabinopyranose-13C5
  • HY-180571
    LUF7996

    		PROTACs CCR Cancer
    LUF7996 is a CCR2 PROTAC Degrader degrading CCR2 with DC50 = 2.6 μM. LUF7996 demonstrates engagement of both and the E3 ligase cereblon and displays sustain and concentration-dependent degradation of CCR2. LUF7996 reliance on the lysosomal pathway to induce CCR2 degradation. LUF7996 efficiently inhibits monocyte migration in virto .
    LUF7996
  • HY-183660
    F-SLOH

    		Autophagy Amyloid-β Tau Protein Neurological Disease
    F-SLOH is a brain-penerant and orally active TFEB activator and amyloid-β inhibitor with an IC50 of 3.4 μM against amyloid-β. F-SLOH promotes nuclear translocation of TFEB, driving autophagy and lysosomal biogenesis. F-SLOH reduces amyloid-β oligomers and Tau aggregates via autophagy lysosomal degradation pathway. F-SLOH can be used for the research of Alzheimer’s disease .
    F-SLOH
  • HY-183907
    Cicletanine

    		Calcium Channel Cardiovascular Disease
    Cicletanine is a voltage-dependent Ca 2+ channel inhibitor. Cicletanine inhibits α-adrenoceptor-mediated Ca 2+ release pathway, and shows vasodilatory effects on isolated vascular smooth muscle. Cicletanine directly stimulates lysosomal and cytoplasmic cholesteryl ester hydrolase activity. Cicletanine can be used for the research of hypertension .
    Cicletanine
  • HY-180222
    KGA-4066

    		CDK Cancer
    KGA-4066 is a novel non-ATP-competitive CDK2 inhibitor. KGA-4066 inhibits CDK2/Cyclin A2 with an IC50 value of 236.7 nM, disrupts their interaction, promots CDK2 degradation via the lysosomal pathway. KGA-4066 has anticancer activity against hepatocellular carcinoma .
    KGA-4066
  • HY-185306
    Morfamquat dichloride

    PP 745

    		 Herbicide Phosphatase β-glucuronidase Metabolic Disease
    Morfamquat dichloride (PP 745) is a bipyridine herbicide. Acute poisoning by Morfamquat dichloride strongly stimulates the reticuloendothelial system, causes lysosomal membrane damage and enzyme leakage, and interferes with the function of hepatocyte Golgi apparatus and related glucose metabolic pathways. Morfamquat dichloride significantly increases the activities of acid phosphatase and β-glucuronidase, exerting toxic effects on mice, while pre-administration of vitamin E alleviates such toxicity .
    Morfamquat dichloride

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