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lipid deposition

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25

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2

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1

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1

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9

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4

Isotope-Labeled Compounds

Cat. No. Product Name Target Research Areas Chemical Structure
  • 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-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-W011927
    4,4'-Sulfonyldiphenol

    Bisphenol S; Bis(4-hydroxyphenyl) sulfone

    		 Estrogen Receptor/ERR Histone Methyltransferase Thyroid Hormone Receptor PI3K Akt mTOR Androgen Receptor Drug Derivative Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    4,4'-Sulfonyldiphenol (Bisphenol S; Bis(4-hydroxyphenyl) sulfone), a substitute for Bisphenol A (HY-18260), is widely used in industrial and consumer products. 4,4'-Sulfonyldiphenol is an oally ative estrogen receptor (ER) agonist and can competitively bind to thyroid hormone receptors (TR) with IC50 values for TRα and TRβ are 2650 μM and 2294 μM respectively, thereby affecting breast development and reducing the expression of androgen receptor (AR) in fetal testes. 4,4'-Sulfonyldiphenol promotes the progression of glioblastoma by upregulating the EZH2 mediated PI3K/AKT/mTOR pathway. Under chronic exposure, 4,4'-Sulfonyldiphenol can cause significant lipid deposition and dyslipidemia in the mouse liver by upregulating JunB and Atf3, and has a role in causing obesity at low doses. 4,4'-Sulfonyldiphenol induces intestinal inflammation by altering the intestinal microbiome. 4,4'-Sulfonyldiphenol accelerates the progression of atherosclerosis in zebrafish embryo larvae .
    4,4'-Sulfonyldiphenol
  • HY-N3686
    D-Arabitol

    		AMPK PGC-1α Metabolic Disease
    D-Arabitol is an orally active D-enantiomer of arabitol. D-Arabitol modulates the composition of gut microbiota, increases short-chain fatty acids, and promotes AMPK-PGC-1α-related browning of white adipose tissue. D-Arabitol improves weight gain, fat accumulation, insulin resistance, lipid deposition and inflammatory responses. D-Arabitol serves as the sole carbon/energy source for Bacillus methanolicus MGA3, a strain that can co-utilize it with mannitol. D-Arabitol is applicable to obesity-related research .
    D-Arabitol
  • HY-N7055
    Trierucin

    Trierucoylglycerol

    		 Drug Derivative Metabolic Disease
    Trierucin (Trierucoylglycerol) is a triester formed by glycerol and erucic acid, which serves as an occlusive skin conditioning agent and non-aqueous thickener in cosmetics. Long-term feeding of Trierucin to rats induces chronic toxicities such as cardiac lipid deposition and fibrosis .
    Trierucin
  • HY-114557
    NSC 90469

    3,5-Diiodo-L-thyronine

    		 JNK NF-κB Sirtuin PGC-1α COX TGF-β Receptor Collagen Metabolic Disease Inflammation/Immunology Endocrinology
    NSC 90469 (3,5-Diiodo-L-thyronine) is an orally active thyroid hormone derivative. NSC 90469 inhibits JNK phosphorylation and NF-κB acetylation, blocks SIRT1 protein expression, induces elevated PGC-1α levels, and stimulates COX activity. NSC 90469 enhances UCP1-mediated thermogenesis, increases hepatic Dio1 activity, inhibits TSH levels and hypothalamic-pituitary-thyroid axis function, enhances lipid metabolism, and regulates energy metabolism via the mitochondrial pathway. NSC 90469 prevents blood glucose reduction, reduces urinary albumin excretion, inhibits renal matrix expansion, decreases TGF-β1 expression, and reduces renal fibronectin and type Ⅳ collagen deposition. NSC 90469 also increases energy expenditure and prevents diet-induced overweight. NSC 90469 can be used in studies related to diabetic nephropathy, hypothyroidism, non-alcoholic fatty liver disease, and diet-induced obesity .
    NSC 90469
  • HY-B1608
    Chromium chloride

    		Cardiovascular Disease Metabolic Disease
    Chromium chloride is a trivalent chromium compound and an essential trace mineral. Chromium chloride enhances insulin-stimulated GLUT4 translocation and glucose uptake in skeletal muscle. Chromium chloride regulates glucose and lipid metabolism, inhibits TNF-α secretion and oxidative stress in monocytes treated with high glucose or H2O2, and reverses hydrogen peroxide-induced cell growth inhibition. Chromium chloride reduces coronary and aortic lipid deposition and serum cholesterol levels in hypercholesterolemic rabbits. Chromium chloride can be used in research related to diabetes and cardiac atherosclerosis .
    Chromium chloride
  • HY-W011927S
    4,4'-Sulfonyldiphenol-d8
    1 Publications Verification

    Bisphenol S (4,4'-Sulfonyldiphenol)-d8

    		 Isotope-Labeled Compounds Estrogen Receptor/ERR Histone Methyltransferase Thyroid Hormone Receptor PI3K Akt mTOR Androgen Receptor Cardiovascular Disease Metabolic Disease Inflammation/Immunology Endocrinology Cancer
    4,4'-Sulfonyldiphenol-d8 (Bisphenol S (4,4'-Sulfonyldiphenol)-d8) is the deuterium labeled 4,4'-Sulfonyldiphenol (HY-W011927).4,4'-Sulfonyldiphenol (Bisphenol S; Bis(4-hydroxyphenyl) sulfone), a substitute for Bisphenol A (HY-18260), is widely used in industrial and consumer products. 4,4'-Sulfonyldiphenol is an estrogen receptor (ER) agonist and can competitively bind to thyroid hormone receptors (TR) with IC50 values for TRα and TRβ are 2650 μM and 2294 μM respectively, thereby affecting breast development and reducing the expression of androgen receptor (AR) in fetal testes. 4,4'-Sulfonyldiphenol promotes the progression of glioblastoma by upregulating the EZH2 mediated PI3K/AKT/mTOR pathway. Under chronic exposure, 4,4'-Sulfonyldiphenol can cause significant lipid deposition and dyslipidemia in the mouse liver by upregulating JunB and Atf3, and has a role in causing obesity at low doses. 4,4'-Sulfonyldiphenol induces intestinal inflammation by altering the intestinal microbiome. 4,4'-Sulfonyldiphenol accelerates the progression of atherosclerosis in zebrafish embryo larvae.
    4,4'-Sulfonyldiphenol-d8
  • HY-N3686R
    D-Arabitol (Standard)

    		Reference Standards AMPK PGC-1α Metabolic Disease
    D-Arabitol (Standard) is the analytical standard of D-Arabitol. This product is intended for research and analytical applications. D-Arabitol is an orally active D-enantiomer of arabitol. D-Arabitol modulates the composition of gut microbiota, increases short-chain fatty acids, and promotes AMPK-PGC-1α-related browning of white adipose tissue. D-Arabitol improves weight gain, fat accumulation, insulin resistance, lipid deposition and inflammatory responses. D-Arabitol serves as the sole carbon/energy source for Bacillus methanolicus MGA3, a strain that can co-utilize it with mannitol. D-Arabitol is applicable to obesity-related research.
    D-Arabitol (Standard)
  • 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-W011927R
    4,4'-Sulfonyldiphenol (Standard)

    Bisphenol S (Standard); Bis(4-hydroxyphenyl) sulfone (Standard)

    		 Reference Standards Estrogen Receptor/ERR Histone Methyltransferase Thyroid Hormone Receptor PI3K Akt mTOR Androgen Receptor Drug Derivative Cardiovascular Disease Metabolic Disease Inflammation/Immunology Endocrinology Cancer
    4,4'-Sulfonyldiphenol (Bisphenol S; Bis(4-hydroxyphenyl) sulfone) (Standard) is the analytical standard of 4,4'-Sulfonyldiphenol (HY-W011927). This product is intended for research and analytical applications. 4,4'-Sulfonyldiphenol, a substitute for Bisphenol A (HY-18260), is widely used in industrial and consumer products. 4,4'-Sulfonyldiphenol is an estrogen receptor (ER) agonist and can competitively bind to thyroid hormone receptors (TR) with IC50 values for TRα and TRβ are 2650 μM and 2294 μM respectively, thereby affecting breast development and reducing the expression of androgen receptor (AR) in fetal testes. 4,4'-Sulfonyldiphenol promotes the progression of glioblastoma by upregulating the EZH2 mediated PI3K/AKT/mTOR pathway. Under chronic exposure, 4,4'-Sulfonyldiphenol can cause significant lipid deposition and dyslipidemia in the mouse liver by upregulating JunB and Atf3, and has a role in causing obesity at low doses. 4,4'-Sulfonyldiphenol induces intestinal inflammation by altering the intestinal microbiome. 4,4'-Sulfonyldiphenol accelerates the progression of atherosclerosis in zebrafish embryo larvae.
    4,4'-Sulfonyldiphenol (Standard)
  • HY-176274
    FASN/SCD-IN-1

    		Fatty Acid Synthase (FASN) Stearoyl-CoA Desaturase (SCD) Reactive Oxygen Species (ROS) Interleukin Related TNF Receptor SOD LDLR Glutathione Peroxidase Metabolic Disease Inflammation/Immunology
    FASN/SCD-IN-1 is a Silybin (HY-N0779A) derivative, an orally active inhibitor of Fatty Acid Synthase (FASN)/Stearoyl-CoA Desaturase (SCD). FASN/SCD-IN-1 has shown in vitro activity in inhibiting lipid deposition, reducing FASN and SCD transcriptional levels, and exhibiting antioxidant, anti-inflammatory, and anti-fibrotic activities. FASN/SCD-IN-1 has demonstrated significant hepatoprotective effects in a rat model of acute liver injury. FASN/SCD-IN-1 ameliorates the pathological features of MASH liver, including steatosis, inflammation, and fibrosis in a mouse model of myeloproliferative steatohepatitis (MASH). FASN/SCD-IN-1 can be used to study MASH .
    FASN/SCD-IN-1
  • HY-185104
    Ginsenoside C-K hexapropionate ester

    		LXR Cardiovascular Disease
    Ginsenoside C-K hexapropionate ester (Structure 2) is a selective agonist of LXRα, with no significant activation effect on LXRβ. Ginsenoside C-K hexapropionate ester upregulates the expression of downstream genes such as ABCA1 by activating LXRα, promoting reverse cholesterol transport, and reducing lipid deposition in macrophage-derived foam cells. It can be used in the research of atherosclerosis. Ginsenoside C-K hexapropionate ester is a derivative synthesized from ginsenoside Compound K, an active metabolite of Panax notoginseng saponins, by modification with propionic anhydride .
    Ginsenoside C-K hexapropionate ester
  • HY-178717
    WML-01

    		Fungal Infection
    WML-01 is a fungicide with EC50s of 0.079, 0.72 and 2.02 μg/mL against F. graminearum, F. fujikuroi and S. sclerotiorum. WML-01 disrupts the cell membrane of F. graminearum and induces deposition of lipid droplets. WML-01 inhibits Deoxynivalenol (DON) (HY-N6684) biosynthesis with no cross-resistance and strongly suppresses ribosomal subunit assembly, impairing protein synthesis. WML-01 effectively controls the fusarium head blight (FHB) epidemic .
    WML-01
  • 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-168639
    AMPK activator 15

    		Mitochondrial Metabolism AMPK Metabolic Disease
    AP39 prodrug 1 (Compound M1) is a mitochondria-targeted H2S prodrug. AP39 prodrug 1 induces ROS-dependent mild mitochondrial uncoupling, activating mitochondria-associated AMPK to suppress Palmitic acid (PA) (HY-N0830)-induced lipid deposition in hepatocytes .
    AMPK activator 15
  • HY-N3686S
    D-Arabitol-13C

    		Isotope-Labeled Compounds AMPK PGC-1α Metabolic Disease
    D-Arabitol- 13C is the 13C labeled D-Arabitol. D-Arabitol is an orally active D-enantiomer of arabitol. D-Arabitol modulates the composition of gut microbiota, increases short-chain fatty acids, and promotes AMPK-PGC-1α-related browning of white adipose tissue. D-Arabitol improves weight gain, fat accumulation, insulin resistance, lipid deposition and inflammatory responses. D-Arabitol serves as the sole carbon/energy source for Bacillus methanolicus MGA3, a strain that can co-utilize it with mannitol. D-Arabitol is applicable to obesity-related research.
    D-Arabitol-13C
  • HY-N3686S1
    D-Arabitol-13C-1

    		Isotope-Labeled Compounds AMPK PGC-1α Metabolic Disease
    D-Arabitol- 13C-1 is the 13C labeled D-Arabitol. D-Arabitol is an orally active D-enantiomer of arabitol. D-Arabitol modulates the composition of gut microbiota, increases short-chain fatty acids, and promotes AMPK-PGC-1α-related browning of white adipose tissue. D-Arabitol improves weight gain, fat accumulation, insulin resistance, lipid deposition and inflammatory responses. D-Arabitol serves as the sole carbon/energy source for Bacillus methanolicus MGA3, a strain that can co-utilize it with mannitol. D-Arabitol is applicable to obesity-related research.
    D-Arabitol-13C-1
  • HY-N3686S2
    D-Arabitol-13C-2

    		Isotope-Labeled Compounds AMPK PGC-1α Metabolic Disease
    D-Arabitol- 13C-2 is the 13C labeled D-Arabitol. D-Arabitol is an orally active D-enantiomer of arabitol. D-Arabitol modulates the composition of gut microbiota, increases short-chain fatty acids, and promotes AMPK-PGC-1α-related browning of white adipose tissue. D-Arabitol improves weight gain, fat accumulation, insulin resistance, lipid deposition and inflammatory responses. D-Arabitol serves as the sole carbon/energy source for Bacillus methanolicus MGA3, a strain that can co-utilize it with mannitol. D-Arabitol is applicable to obesity-related research.
    D-Arabitol-13C-2
  • HY-125533
    TXA497

    		Bacterial Infection
    TXA497 is a potent local topical bactericide. TXA497 exerts its bactericidal effect by interfering with the polymerization kinetics of the bacterial cell division protein FtsZ, rather than inhibiting it. TXA497 shows strong activity against various Staphylococcus aureus strains, including MRSA and MSSA, with an MIC value ranging from 1.0 to 2.0 μg/mL. TXA497 skin deposition is concentration-dependent in its formulation, consistent with Fick's first law. TXA497 has limited systemic permeability through the lipid pathway of the stratum corneum and is easily absorbed through this route. TXA497 can be used for research on topical bactericidal agents .
    TXA497
  • 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
  • HY-114557R
    NSC 90469 (Standard)

    3,5-Diiodo-L-thyronine (Standard)

    		 Reference Standards Endogenous Metabolite Metabolic Disease
    NSC 90469 (Standard) is the analytical standard of NSC 90469. This product is intended for research and analytical applications. NSC 90469 (3,5-Diiodo-L-thyronine) is an orally active thyroid hormone derivative. NSC 90469 inhibits JNK phosphorylation and NF-κB acetylation, blocks SIRT1 protein expression, induces elevated PGC-1α levels, and stimulates COX activity. NSC 90469 enhances UCP1-mediated thermogenesis, increases hepatic Dio1 activity, inhibits TSH levels and hypothalamic-pituitary-thyroid axis function, enhances lipid metabolism, and regulates energy metabolism via the mitochondrial pathway. NSC 90469 prevents blood glucose reduction, reduces urinary albumin excretion, inhibits renal matrix expansion, decreases TGF-β1 expression, and reduces renal fibronectin and type Ⅳ collagen deposition. NSC 90469 also increases energy expenditure and prevents diet-induced overweight. NSC 90469 can be used in studies related to diabetic nephropathy, hypothyroidism, non-alcoholic fatty liver disease, and diet-induced obesity .
    NSC 90469 (Standard)
  • HY-P11588
    KBP-042

    		Amylin Receptor CGRP Receptor Metabolic Disease
    KBP-042 is an orally active amylin receptor activator, a calcitonin receptor activator. KBP-042 induces sustained weight loss, reduces adipose tissue mass, lowers hepatic lipid deposition, increases plasma adiponectin, decreases plasma leptin, and reduces plasma glucose-dependent insulinotropic peptide levels. KBP-042 can be used for the research of obesity and insulin resistance .
    KBP-042
  • HY-183949
    Insecticidal agent 33

    		Insecticide Cholinesterase (ChE) Reactive Oxygen Species (ROS) Infection
    Insecticidal agent 33 is an AChE inhibitor with nematicidal activity. Insecticidal agent 33 impairs locomotor activity of Caenorhabditis elegans, and induces oxidative damage in Caenorhabditis elegans, including elevated reactive oxygen species (ROS) levels, lipofuscin accumulation, lipid deposition, and disrupted cellular homeostasis. Insecticidal agent 33 can be used for the research of plant-parasitic nematode infection .
    Insecticidal agent 33
  • HY-184158
    HATC

    		AUTACs HIF/HIF Prolyl-Hydroxylase Metabolic Disease Inflammation/Immunology
    HATC is a HIF-1α AUTAC degrader. HATC links HIF-1α to LC3 to form a ternary complex that undergoes degradation via the autophagy-lysosome fusion pathway. HATC induces dose-dependent HIF-1α degradation in multiple cell types. HATC reduces visceral fat accumulation, hepatic lipid deposition, senescent cell aggregation, and bone loss; alleviates age-related intervertebral disc degeneration, liver dysfunction, kyphosis, and alveolar dilation; decreases circulating lactic acid levels; improves physical performance; and reverses age-related changes in granulocyte proportions. HATC extends median and maximum lifespan, reduces transcriptomic age, and causes no obvious persistent toxicity. HATC can be used in the research of age-related diseases (pink: LC3 ligand (HY-50759); blue: HIF-1α ligand (HY-P10426); Linker: (HY-W008264)) .
    HATC

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