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Pathways Recommended:	Stem Cell/Wnt Cell Cycle/DNA Damage

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normal human liver cells

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By Targets:	Acyltransferase (1) Androgen Receptor (1) Apoptosis (7) Bacterial (1) Bcl-2 Family (1) BCL6 (4) Caspase (6) COX (1) DNA/RNA Synthesis (1) Drug Derivative (2) Drug Metabolite (1) EGFR (1) Endogenous Metabolite (4) Histone Methyltransferase (1) Interleukin Related (6) Lipoxygenase (1) PAK (1) Parasite (1) PARP (2) Phosphodiesterase (PDE) (1) Pim (1) PROTACs (2) Reference Standards (3) STAT (4)
By Research Areas:	Cancer (13) Cardiovascular Disease (1) Infection (2) Inflammation/Immunology (3) Metabolic Disease (6)

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Screening Libraries

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Targets Recommended: LXR Nuclear Factor of activated T Cells (NFAT) TREM receptor

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) .

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) .

HY-W089800

trans-2-Nonenal trans-2-Nonen-1-al	COX Lipoxygenase Apoptosis	Cardiovascular Disease Inflammation/Immunology
trans-2-Nonenal (trans-2-Nonen-1-al) is an endogenous peroxidation product of polyunsaturated fatty acids, acting as an inhibitor of COX and 12-LOX, as well as an inducer of apoptosis. trans-2-Nonenal is also a malodorous compound secreted by the human body, and its content gradually increases with aging. trans-2-Nonenal inhibits the activities of multiple enzymes such as platelet membrane-bound PTPase, preferentially covalently modifies proteins at lysine residues to form immunogenic adducts, and regulates platelet Arachidonic acid (HY-109590) metabolism. trans-2-Nonenal also exhibits significant cytotoxicity, reduces the viability of keratinocytes, promotes their apoptosis, and effectively decreases the thickness of epidermal models and the number of proliferating cells. trans-2-Nonenal is commonly used in studies of thrombotic, atherosclerotic diseases, renal adenocarcinoma, etc. .

HY-112487

Sandoz 58-035	Acyltransferase	Metabolic Disease
Sandoz 58-035 is a selective acyl-CoA:cholesterol acyltransferase (ACAT) inhibitor. Sandoz 58-035 inhibits this enzyme in intact cells and isolated microsomal fractions. Sandoz 58-035 blocks the esterification of exogenous vesicle-derived cholesterol and the incorporation of oleic acid into cellular cholesterol esters, reducing the formation and accumulation of cholesterol esters. Sandoz 58-035 causes a slight increase in cellular free cholesterol, and at high concentrations, it also causes a slight reduction in overall cellular protein synthesis. Sandoz 58-035 can be used in studies related to cellular cholesterol regulation .

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].

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) .

HY-176128

BWA-6047	PROTACs Androgen Receptor Apoptosis PARP Caspase	Cancer
BWA-6047 is an oral active PROTAC degrader targeting AR/AR-V7 and GSPT1 with DC₅₀ values of 3.7, 3.0 and 1.2 nM in 22Rv1 cells. BWA-6047 suppresses the expression of AR downstream target genes and and transcriptional activity. BWA-6047 inhibits cancer cells proliferation, causes G1 phase cell cycle arrest and induces apoptosis. BWA-6047 increases cleaved-PARP-1 and cleaved-caspase-3 levels. BWA-6047 reduces growth of LNCaP xenograft tumors in mice models without obvious toxicity. BWA-6047 can be used for the research of prostate cancer .

HY-157404

Pim-1/2 kinase inhibitor 2	Pim	Cancer
Pim-1/2 kinase inhibitor 2 (compound 5b) is a competitive PIM-1 and PIM-2 kinase inhibitor with IC₅₀s of 1.31 μM and 0.67 μM, respectively. Pim-1/2 kinase inhibitor 2 shows in-vitro low cytotoxicity against normal human lung fibroblast Wi-38 cell line and potent in-vitro anticancer activity against myeloid leukaemia (NFS-60), liver (HepG-2), prostate (PC-3), and colon (Caco-2) cancer cell lines .

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) .

HY-182784

Antibacterial agent 336	Bacterial	Infection
Antibacterial agent 336 is an antibacterical agent with broad-spectrum inhibitory activity against Gram-negative and Gram-positive bacteria. Antibacterial agent 336 binds tightly via its pyridine group to the carboxyl group, Lys-465 residue, and Leu-480 residue of the MsbA protein, interfering with bacterial outer membrane synthesis, and exerts concentration-dependent bactericidal activity against bacterial. Antibacterial agent 336 has low cytotoxicity to normal human liver cells. Antibacterial agent 336 can be used for the research of bacterial infections .

HY-183716

Mito-TP-2	Drug Derivative	Cancer
Mito-TP-2 is a triptolide (HY-32735) derivative. Mito-TP-2 exhibits concentration-dependent cytotoxicity in cancer cells. Mito-TP-2 is selectively driven and accumulated into the mitochondria of tumor cells by mitochondrial transmembrane potential and exerts specific mitochondrial toxicity. Mito-TP-2 can be used for the research of liver cancer, breast cancer, and non-small cell lung cancer .

HY-181142

Antitumor agent-213	EGFR Apoptosis	Cancer
Antitumor agent-213 is an antitumor agent. Antitumor agent-213 binds to epidermal growth factor receptor (EGFR) and shows antitumor activity. Antitumor agent-213 can inhibit cancer cells proliferation, migration and induces apoptosis. Antitumor agent-213 can be used for the research of cancer, such as liver cancer .

HY-181088

PDE3/4-IN-4	Phosphodiesterase (PDE) Interleukin Related	Metabolic Disease
PDE3/4-IN-4 is an orally active PDE3A and PDE4B inhibitor with IC₅₀ values of 10 nM and 9.4 nM, respectively. PDE3/4-IN-4 shows selective activity relative to most other PDE family members. PDE3/4-IN-4 modulates the cAMP/PKA/CREB signaling pathway. PDE3/4-IN-4 inhibits pro-inflammatory factor IL-6. PDE3/4-IN-4 reduces expression of inflammatory markers in liver tissue. PDE3/4-IN-4 attenuates liver fibrosis. PDE3/4-IN-4 limits liver damage in cholestatic and sepsis-induced liver disease mice models. PDE3/4-IN-4 can be used for the research of liver injury, cholestatic liver diseases, sepsis-induced liver injury .

HY-W743094

Methylstenbolone	Drug Derivative	Inflammation/Immunology Cancer
Methylstenbolone is a steroid and an anti-inflammatory agent. Methylstenbolone inhibits nitric oxide production in macrophages and exhibits cytotoxicity against breast cancer cells and normal fibroblasts. Methylstenbolone can be used for the research of inflammation and breast cancer .

HY-181827

IL-17-IN-7	Interleukin Related	Inflammation/Immunology
IL-17-IN-7 (Compound 23) is a IL-17 inhibitor with a pIC₅₀ of 7.1 against IL-17A .

HY-123599

IACS-4619	DNA/RNA Synthesis	Cancer
IACS-4619 (compound 4) is a highly selective 2-aminopyrimidine-based MTH1 (MutT homolog 1) inhibitor (IC₅₀=0.2 nM). IACS-4619 inhibits MTH1 by blocking its hydrolysis of oxidized purine nucleotides such as 8-oxo-dGTP, thereby preventing MTH1 from inhibiting the incorporation of oxidized nucleotides into DNA. IACS-4619 significantly inhibits endogenous MTH1 activity in MTH1-overexpressing U2OS cells, but without antiproliferative or cytotoxic effects on various human cancer and normal cell lines. IACS-4619 can be used in oncology research related to the MTH1 target .

HY-118606

LDN-0044878	PAK Parasite	Infection Cancer
LDN-0044878 is a PAK3 inhibitor. LDN-0044878 inhibits the proliferation or induces the death of p53-deficient cells. LDN-0044878 exhibits moderate trypanocidal activity against Trypanosoma brucei, but does not directly inhibit the core target Rhodesain. LDN-0044878 can be used in studies related to cervical adenocarcinoma and Trypanosoma brucei infection.

HY-181413

PROTAC EZH2 Degrader-44	PROTACs Histone Methyltransferase Bcl-2 Family Caspase PARP	Cancer
PROTAC EZH2 Degrader-44 (compound 60) is a highly efficient PROTAC degrader targeting the EZH2-PRC2 complex. By recruiting the CRBN E3 ligase and relying on the proteasome system, PROTAC EZH2 Degrader-44 simultaneously induces the degradation of core components EZH2, SUZ12 and EED, thereby significantly reducing the levels of H3K27me3 and CARM1. PROTAC EZH2 Degrader-44 exerts antiproliferative effects through a dual mechanism: on the one hand, it triggers mitochondrial dysfunction leading to decreased membrane potential; on the other hand, it strongly promotes apoptosis by regulating Bcl-2 family proteins (upregulating Bax, Caspase-3 and PARP, and downregulating Bcl-2). PROTAC EZH2 Degrader-44 exhibits only extremely low cytotoxicity in human normal mammary epithelial, liver and kidney cells, showing a favorable safety window. PROTAC EZH2 Degrader-44 is an ideal tool molecule for exploring the mechanisms of targeted therapy for triple-negative breast cancer .

Cat. No.	Product Name

HY-L228

Lipid Metabolite Compound Library	145 compounds
Lipids are important energy storage substances in the human body. They are involved in the regulation of cell structure and function, as well as signaling pathways and gene expression. Abnormal lipid levels in tissues or their dysregulation can lead to various diseases. These include obesity, type 2 diabetes, non-alcoholic fatty liver disease, neurodegenerative diseases, infections, and cancer. Therefore, maintaining normal levels of lipid metabolism is critical to overall health. One of the key features of cancer is aberrant lipid metabolism. This includes alterations in lipid uptake, lipid desaturation, neolipogenesis, lipid droplets, and fatty acid oxidation in cancer cells. These changes all contribute to cellular survival in an ever-changing microenvironment. They do this by modulating feed-forward oncogenic signals and key oncogenic functions. Additionally, they affect oxidative stress, other types of stress, immune responses, and intercellular communication. Alterations in lipid metabolism have a strong impact on the properties of cancer stem cells. This includes aspects such as self-renewal, differentiation, invasion, metastasis, drug sensitivity, and resistance. Furthermore, these alterations also modulate T cell responses. MCE can offer 145 metabolites of lipid metabolism pathways, which can be used for drug screening in cancer, immune-based diseases, metabolic diseases, and other diseases.

Lipid Metabolite Compound Library

145 compounds

Lipids are important energy storage substances in the human body. They are involved in the regulation of cell structure and function, as well as signaling pathways and gene expression. Abnormal lipid levels in tissues or their dysregulation can lead to various diseases. These include obesity, type 2 diabetes, non-alcoholic fatty liver disease, neurodegenerative diseases, infections, and cancer. Therefore, maintaining normal levels of lipid metabolism is critical to overall health.

One of the key features of cancer is aberrant lipid metabolism. This includes alterations in lipid uptake, lipid desaturation, neolipogenesis, lipid droplets, and fatty acid oxidation in cancer cells. These changes all contribute to cellular survival in an ever-changing microenvironment. They do this by modulating feed-forward oncogenic signals and key oncogenic functions. Additionally, they affect oxidative stress, other types of stress, immune responses, and intercellular communication. Alterations in lipid metabolism have a strong impact on the properties of cancer stem cells. This includes aspects such as self-renewal, differentiation, invasion, metastasis, drug sensitivity, and resistance. Furthermore, these alterations also modulate T cell responses.

MCE can offer 145 metabolites of lipid metabolism pathways, which can be used for drug screening in cancer, immune-based diseases, metabolic diseases, and other diseases.

Cat. No.	Product Name	Type

HY-W089800

trans-2-Nonenal trans-2-Nonen-1-al	Biochemical Assay Reagents
trans-2-Nonenal (trans-2-Nonen-1-al) is an endogenous peroxidation product of polyunsaturated fatty acids, acting as an inhibitor of COX and 12-LOX, as well as an inducer of apoptosis. trans-2-Nonenal is also a malodorous compound secreted by the human body, and its content gradually increases with aging. trans-2-Nonenal inhibits the activities of multiple enzymes such as platelet membrane-bound PTPase, preferentially covalently modifies proteins at lysine residues to form immunogenic adducts, and regulates platelet Arachidonic acid (HY-109590) metabolism. trans-2-Nonenal also exhibits significant cytotoxicity, reduces the viability of keratinocytes, promotes their apoptosis, and effectively decreases the thickness of epidermal models and the number of proliferating cells. trans-2-Nonenal is commonly used in studies of thrombotic, atherosclerotic diseases, renal adenocarcinoma, etc. .

trans-2-Nonenal

trans-2-Nonen-1-al

Biochemical Assay Reagents

trans-2-Nonenal (trans-2-Nonen-1-al) is an endogenous peroxidation product of polyunsaturated fatty acids, acting as an inhibitor of COX and 12-LOX, as well as an inducer of apoptosis. trans-2-Nonenal is also a malodorous compound secreted by the human body, and its content gradually increases with aging. trans-2-Nonenal inhibits the activities of multiple enzymes such as platelet membrane-bound PTPase, preferentially covalently modifies proteins at lysine residues to form immunogenic adducts, and regulates platelet Arachidonic acid (HY-109590) metabolism. trans-2-Nonenal also exhibits significant cytotoxicity, reduces the viability of keratinocytes, promotes their apoptosis, and effectively decreases the thickness of epidermal models and the number of proliferating cells. trans-2-Nonenal is commonly used in studies of thrombotic, atherosclerotic diseases, renal adenocarcinoma, etc. .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-N2334

Glycochenodeoxycholic acid 5 Publications Verification Chenodeoxycholylglycine	Microorganisms Classification of Application Fields Endogenous metabolite Disease Research Fields Steroids Source Classification Cancer	Endogenous Metabolite Apoptosis STAT BCL6 Interleukin Related Caspase
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) .

HY-N2334A

Glycochenodeoxycholic acid sodium salt 5 Publications Verification Chenodeoxycholylglycine sodium salt; Sodium glycochenodeoxycholate	Classification of Application Fields Endogenous metabolite Disease Research Fields Steroids Source Classification Cancer	Endogenous Metabolite Apoptosis STAT BCL6 Interleukin Related Caspase
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) .

HY-W089800

trans-2-Nonenal trans-2-Nonen-1-al	Source Classification	COX Lipoxygenase Apoptosis
trans-2-Nonenal (trans-2-Nonen-1-al) is an endogenous peroxidation product of polyunsaturated fatty acids, acting as an inhibitor of COX and 12-LOX, as well as an inducer of apoptosis. trans-2-Nonenal is also a malodorous compound secreted by the human body, and its content gradually increases with aging. trans-2-Nonenal inhibits the activities of multiple enzymes such as platelet membrane-bound PTPase, preferentially covalently modifies proteins at lysine residues to form immunogenic adducts, and regulates platelet Arachidonic acid (HY-109590) metabolism. trans-2-Nonenal also exhibits significant cytotoxicity, reduces the viability of keratinocytes, promotes their apoptosis, and effectively decreases the thickness of epidermal models and the number of proliferating cells. trans-2-Nonenal is commonly used in studies of thrombotic, atherosclerotic diseases, renal adenocarcinoma, etc. .

HY-N2334R

Glycochenodeoxycholic acid (Standard) Chenodeoxycholylglycine (Standard)	Structural Classification Microorganisms Endogenous metabolite Steroids Source Classification	Reference Standards Endogenous Metabolite Apoptosis STAT BCL6 Interleukin Related Caspase
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].

HY-N2334AR

Glycochenodeoxycholic acid sodium salt (Standard) Chenodeoxycholylglycine sodium salt (Standard); Sodium glycochenodeoxycholate (Standard)	Structural Classification Endogenous metabolite Steroids Source Classification	Reference Standards Endogenous Metabolite Apoptosis STAT BCL6 Interleukin Related Caspase
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) .

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normal human liver cells

Inhibitors & Agonists

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