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

Results for "

tumor cell necroptosis

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Necroptosis (9) 11β-HSD (2) Akt (3) Aldehyde Dehydrogenase (ALDH) (1) AMPK (2) Apoptosis (10) Autophagy (6) Bcl-2 Family (1) Btk (1) Caspase (3) Epigenetic Reader Domain (1) ERK (2) Ferroptosis (3) Histone Methyltransferase (4) Keap1-Nrf2 (2) Mitochondrial Metabolism (1) Mixed Lineage Kinase (1) NF-κB (1) p38 MAPK (3) PANoptosis (1) PARP (3) Photosensitizer (1) PI3K (2) Reactive Oxygen Species (ROS) (3) Reference Standards (3) RIP kinase (1) STING (2) Transferrin Receptor (1) TRP Channel (1) TrxR (1) VEGFR (2) β-catenin (1)
By Research Areas:	Cancer (20) Inflammation/Immunology (3) Metabolic Disease (3) Neurological Disease (3)

By Targets:

Necroptosis (9)

11β-HSD (2)

Akt (3)

Aldehyde Dehydrogenase (ALDH) (1)

AMPK (2)

Apoptosis (10)

Autophagy (6)

Bcl-2 Family (1)

Btk (1)

Caspase (3)

Epigenetic Reader Domain (1)

ERK (2)

Ferroptosis (3)

Histone Methyltransferase (4)

Keap1-Nrf2 (2)

Mitochondrial Metabolism (1)

Mixed Lineage Kinase (1)

NF-κB (1)

p38 MAPK (3)

PANoptosis (1)

PARP (3)

Photosensitizer (1)

PI3K (2)

Reactive Oxygen Species (ROS) (3)

Reference Standards (3)

RIP kinase (1)

STING (2)

Transferrin Receptor (1)

TRP Channel (1)

TrxR (1)

VEGFR (2)

β-catenin (1)

By Research Areas:

Cancer (20)

Inflammation/Immunology (3)

Metabolic Disease (3)

Neurological Disease (3)

Inhibitors & Agonists

Screening Libraries

Natural
Products

Targets Recommended: Necroptosis Large Tumor Suppressor (LATS) TNF Receptor BRK Programmed Cell Death 4 (PDCD4) Itk TOPK NAMPT ALCAM/CD166 GDNF Receptor BCL6 Tim3 VISTA BMI1

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-18768

NCT-501 5 Publications Verification	Aldehyde Dehydrogenase (ALDH) Akt β-catenin Necroptosis	Cancer
NCT-501 is a reversible, non-competitive, selective, blood-brain barrier-permeable ALDH1A1 inhibitor with an IC₅₀ of 40 nM. NCT-501 inhibits the AKT-β-catenin signaling pathway, induces necroptosis in nasopharyngeal carcinoma cells, suppresses their proliferation and inhibits stem cell spheroid formation. NCT-501 can be used in research related to nasopharyngeal carcinoma, esophageal squamous cell carcinoma and malignant tumors .

HY-10587

BIX-01294 Maximum Cited Publications 27 Publications Verification	Histone Methyltransferase Autophagy	Cancer
BIX-01294 is a reversible and highly selective G9a and GLP Histone Methyltransferase inhibitor, with IC₅₀s of of 1.7 μM and 0.9 μM, respectively. BIX-01294 inhibits G9a/GLP by competing for binding with the amino acids N-terminal of the substrate lysine residue. BIX-01294, a (1H-1,4-diazepin-1-yl)-quinazolin-4-yl amine derivative, induces *necroptosis* and autophagy. BIX-01294 has antitumor activity in recurrent tumor cells .

HY-111838A

ZZW-115 hydrochloride 4 Publications Verification	Apoptosis	Cancer
ZZW-115 hydrochloride is a potent NUPR1 inhibitor, with a K_d of 2.1 μM. ZZW-115 hydrochloride induces tumor cell death by necroptosis and apoptosis. Anticancer activity .

HY-N10319

Artepillin C	Epigenetic Reader Domain Necroptosis TRP Channel	Metabolic Disease Inflammation/Immunology Cancer
Artepillin C is an orally active CREB/CRTC2 inhibitor and TRPA1 covalent agonist (EC₅₀=1.8 μM). Artepillin C inhibits CREB/CRTC2-mediated gene transcription and downregulates BMAL1 expression to regulate glucose and lipid metabolism. Artepillin C can also activate TRPA1 channels to induce spicy taste signals. Artepillin C can inhibit tumor cell proliferation, induce *necroptosis, improve insulin resistance and inhibit liver lipid synthesis. Artepillin C can be used in the study of metabolic syndrome, tumor* prevention and treatment, and inflammation .

HY-N0660

Jujuboside B	Apoptosis PARP Caspase AMPK Autophagy VEGFR Keap1-Nrf2 STING 11β-HSD Ferroptosis PI3K Akt p38 MAPK ERK	Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Jujuboside B is a bioactive saponin component isolated from Ziziphi Spinosae Semen (sour jujube seed), with oral efficacy and blood-brain barrier permeability. Jujuboside B induces acute leukemia cell death and drives necroptosis apoptosis by activating the RIPK1/RIPK3/MLKL pathway. Jujuboside B upregulates the expression of NOXA, PARP and caspase-3, activates AMPK, inhibits the proliferation of breast cancer cells, and induces cell apoptosis and autophagy. Jujuboside B inhibits angiogenesis and tumor growth by blocking the VEGFR-2 signaling pathway. Jujuboside B alleviates liver injury in mice by regulating the Nrf2-STING signaling pathway . Jujuboside B alleviates liver injury by regulating anti-inflammatory responses and downregulating the expression of 11β-HSD2. Jujuboside B induces ferroptosis and overcomes radioresistance in non-small cell lung cancer via the PPARγ-ATF3-Gpx4 signaling pathway. Jujuboside B exerts inhibitory effects on platelet aggregation. Jujuboside B inhibits febrile seizures by suppressing the activity of AMPA receptors. Jujuboside B reverses chronic unpredictable mild stress-promoted tumor progression by blocking the PI3K/Akt and MAPK/ERK pathways and dephosphorylating CREB signaling. Jujuboside B is applicable to related studies on acute leukemia, breast cancer, PM_2.5-induced lung injury, hepatotoxicity, liver injury, colorectal cancer, non-small cell lung cancer, thromboembolic diseases, cardiovascular diseases associated with high platelet aggregation, febrile seizures, and depressive-like phenotypes .

HY-159569

TfR-1-IN-1 1 Publications Verification	Transferrin Receptor Ferroptosis Apoptosis Necroptosis	Cancer
TfR-1-IN-1 is a transferrin receptor-1 (TfR-1) inhibitor with tumor cell-specific activity. TfR-1-IN-1 reduces TfR-1 expression, impairs mitochondrial function, induces cell apoptosis, *necroptosis* and ferroptosis, and increases intracellular iron (II) levels. TfR-1-IN-1 decreases the metabolic activity of cancer cells. TfR-1-IN-1 can be used for the research of ovarian cancer, breast cancer and acute myeloid leukemia .

HY-111838

ZZW-115 4 Publications Verification	Apoptosis	Cancer
ZZW-115 is a potent NUPR1 inhibitor, with a K_d of 2.1 μM. ZZW-115 induces tumor cell death by necroptosis and apoptosis. Anticancer activity .

HY-108239

BIX-01294 trihydrochloride Maximum Cited Publications 27 Publications Verification	Histone Methyltransferase Autophagy	Cancer
BIX-01294 trihydrochloride is a reversible and highly selective G9a and GLP Histone Methyltransferase inhibitor, with IC₅₀s of of 1.7 μM and 0.9 μM, respectively. BIX-01294 trihydrochloride inhibits G9a/GLP by competing for binding with the amino acids N-terminal of the substrate lysine residue. BIX-01294 trihydrochloride, a (1H-1,4-diazepin-1-yl)-quinazolin-4-yl amine derivative, induces *necroptosis* and autophagy. BIX-01294 trihydrochloride has antitumor activity in recurrent tumor cells .

HY-169023

Antiangiogenic agent 6	Apoptosis	Cancer
Antiangiogenic agent 6 (Pt-1) can inhibit angiogenesis. Antiangiogenic agent 6 can induce necroptosis in tumor cells .

HY-121261

Antineoplastic agent-1	Necroptosis Apoptosis	Cancer
Antineoplastic agent-1 is an alkylating agent and a genotoxic agent that can induce DNA damage. Antineoplastic agent-1 can lead to irreversible damage and progressive death of liver cells due to *necroptosis* and apoptosis. Antineoplastic agent-1 can cause alkylation damage to hematopoietic cells and stromal cells in the bone marrow. Antineoplastic agent-1 can be used in tumor research .

HY-176219

Bcl-2-IN-23	Bcl-2 Family Apoptosis Necroptosis	Cancer
Bcl-2-IN-23 (compound 5) is a selective inhibitor targeting Bcl-2. The IC₅₀ of Bcl-2-IN-23 in HTB-140, HeLa and SW620 cells is 25.7-33.7 μM. Bcl-2-IN-23 can non-covalently competitively bind to Bcl-2 protein, significantly reduce its expression, and induce late apoptosis and *necroptosis* of cancer cells. Bcl-2-IN-23 enhances the sensitivity of cancer cells to apoptosis and reduces the release of IL-6 inflammatory factors by disrupting the Bcl-2-mediated mitochondrial apoptosis inhibition pathway. Bcl-2-IN-23 can be used for anti-apoptosis research of malignant tumors such as melanoma, cervical cancer, and colorectal cancer .

HY-183797

Antitumor agent-218	Photosensitizer Reactive Oxygen Species (ROS) Necroptosis	Cancer
Antitumor agent-218 is an aggregation-induced emission (AIE)-based photosensitizer. Antitumor agent-218 selectively accumulates in the endoplasmic reticulum, and generates ROS within the endoplasmic reticulum upon irradiation to induce necroptosis of tumor cells. Antitumor agent-218 can be used in cancer-related research .

HY-181718

Necroptosis inducer 1	Necroptosis TrxR Reactive Oxygen Species (ROS)	Cancer
Necroptosis inducer 1 is a *necroptosis* inducer. Necroptosis inducer 1 inhibits the activity of thioredoxin reductase (TrxR), elevates intracellular ROS levels, triggers ROS-mediated necroptosis, and induces necroptosis-dependent immunogenic cell death. Necroptosis inducer 1 inhibits tumor growth, remodels the tumor immune microenvironment, and exerts a synergistic effect with anti-PD-1 in animal models. Necroptosis inducer 1 is applicable to the research of colon cancer .

HY-183538

Necroptosis inducer 2	Necroptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism Mixed Lineage Kinase RIP kinase	Cancer
Necroptosis inducer 2 is a *necroptosis* inducer and copper chelator. Necroptosis inducer 2 chelates intracellular free copper ions, disrupts redox homeostasis, elevates ROS levels, disrupts mitochondrial membrane potential, and induces cancer cell necroptosis. Necroptosis inducer 2 upregulates the necroptosis markers p-MLKL and p-RIP3 expression. Necroptosis inducer 2 exhibits anti-tumor activity in mice. Necroptosis inducer 2 can be used for the research of cancer, such as triple-negative breast cancer .

HY-181073

Apoptosis/necroptosis inducer 1	Apoptosis Necroptosis NF-κB p38 MAPK	Neurological Disease Cancer
Apoptosis/necroptosis inducer 1 is an orally active and brain-penetrant apoptosis and *necroptosis* inducer. Apoptosis/necroptosis inducer 1 induces mitochondria-dependent (intrinsic pathway) apoptosis. Apoptosis/necroptosis inducer 1 induces necroptosis by activating the TNF-α/NF-κB/MAPK signaling pathway. Apoptosis/necroptosis inducer 1 exhibits antiproliferative activity in glioblastoma cell lines and multiple solid tumor types. Apoptosis/necroptosis inducer 1 inhibits growth of orthotopic glioblastoma in animal models and improves survival rate. Apoptosis/necroptosis inducer 1 can be used for the research of glioblastoma .

HY-181996

BTK-IN-47	Btk Caspase Apoptosis PARP	Cancer
BTK-IN-47 (Compound 9e) is a covalent, selective BTK inhibitor with an IC₅₀ of 5.15 nM against BTK. BTK-IN-47 inhibits the BTK signaling pathway, induces cell cycle arrest, and activates the canonical Caspase-dependent Apoptotic pathway (promoting the cleavage of Caspase-3, Caspase-7 and PARP), without inducing necroptosis, pyroptosis or ferroptosis. BTK-IN-47 exerts dose-dependent antiproliferative activity against hematologic tumor cell lines. BTK-IN-47 exhibits dose-dependent in vivo antitumor activity in a Ramos cell xenograft model in BALB/c nude mice. BTK-IN-47 can be used for the research of hematologic malignancies .

HY-182066

Photosensitizer-9	PANoptosis	Cancer
Photosensitizer-9 is an iridium (III)-based photosensitizer with anti-melanoma activity. Photosensitizer-9 exhibits significant phototoxicity (IC₅₀=0.98 μM) and an ideal phototoxicity index (PI=3.05). Under light irradiation, Photosensitizer-9 generates large amounts of intracellular •OH in an oxygen-independent manner. Photosensitizer-9 mediates photodynamic therapy under hypoxic conditions and synergistically activates PANoptosis (by upregulating cleaved Caspase-3, GSDMD-N, p-MLKL), ferroptosis (by disrupting the GSH-GPX4-LPO axis), apoptosis, pyroptosis and necroptosis in melanoma cells. Photosensitizer-9 induces immunogenic cell death by promoting the release of damage-associated molecular patterns under hypoxic conditions and increases the maturation rate of dendritic cells. Photosensitizer-9 reduces tumor volume in melanoma-bearing mice. Photosensitizer-9 is applicable to relevant studies on melanoma .

HY-10587R

BIX-01294 (Standard)	Reference Standards Histone Methyltransferase Autophagy	Cancer
BIX-01294 (Standard) is the analytical standard of BIX-01294 (HY-10587). This product is intended for research and analytical applications. BIX-01294 is a reversible and highly selective G9a and GLP Histone Methyltransferase inhibitor, with IC₅₀s of of 1.7 μM and 0.9 μM, respectively. BIX-01294 inhibits G9a/GLP by competing for binding with the amino acids N-terminal of the substrate lysine residue. BIX-01294, a (1H-1,4-diazepin-1-yl)-quinazolin-4-yl amine derivative, induces necroptosis and autophagy. BIX-01294 has antitumor activity in recurrent tumor cells .

HY-108239R

BIX-01294 trihydrochloride (Standard)	Reference Standards Histone Methyltransferase Autophagy	Cancer
BIX-01294 trihydrochloride (Standard) is the analytical standard of BIX-01294 (trihydrochloride) (HY-108239). This product is intended for research and analytical applications. BIX-01294 trihydrochloride is a reversible and highly selective G9a and GLP Histone Methyltransferase inhibitor, with IC₅₀s of of 1.7 μM and 0.9 μM, respectively. BIX-01294 trihydrochloride inhibits G9a/GLP by competing for binding with the amino acids N-terminal of the substrate lysine residue. BIX-01294 trihydrochloride, a (1H-1,4-diazepin-1-yl)-quinazolin-4-yl amine derivative, induces necroptosis and autophagy. BIX-01294 trihydrochloride has antitumor activity in recurrent tumor cells .

HY-N0660R

Jujuboside B (Standard)	Reference Standards ERK p38 MAPK Akt PI3K 11β-HSD STING VEGFR Ferroptosis Autophagy Apoptosis Keap1-Nrf2 Caspase PARP AMPK	Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Jujuboside B (Standard) is the analytical standard of Jujuboside B. This product is intended for research and analytical applications. Jujuboside B is a bioactive saponin component isolated from Ziziphi Spinosae Semen (sour jujube seed), with oral efficacy and blood-brain barrier permeability. Jujuboside B induces acute leukemia cell death and drives necroptosis apoptosis by activating the RIPK1/RIPK3/MLKL pathway. Jujuboside B upregulates the expression of NOXA, PARP and caspase-3, activates AMPK, inhibits the proliferation of breast cancer cells, and induces cell apoptosis and autophagy. Jujuboside B inhibits angiogenesis and tumor growth by blocking the VEGFR-2 signaling pathway. Jujuboside B alleviates liver injury in mice by regulating the Nrf2-STING signaling pathway . Jujuboside B alleviates liver injury by regulating anti-inflammatory responses and downregulating the expression of 11β-HSD2. Jujuboside B induces ferroptosis and overcomes radioresistance in non-small cell lung cancer via the PPARγ-ATF3-Gpx4 signaling pathway. Jujuboside B exerts inhibitory effects on platelet aggregation. Jujuboside B inhibits febrile seizures by suppressing the activity of AMPA receptors. Jujuboside B reverses chronic unpredictable mild stress-promoted tumor progression by blocking the PI3K/Akt and MAPK/ERK pathways and dephosphorylating CREB signaling. Jujuboside B is applicable to related studies on acute leukemia, breast cancer, PM_2.5-induced lung injury, hepatotoxicity, liver injury, colorectal cancer, non-small cell lung cancer, thromboembolic diseases, cardiovascular diseases associated with high platelet aggregation, febrile seizures, and depressive-like phenotypes.

Cat. No.	Product Name

HY-L133

Cuproptosis Compound Library	419 compounds
Copper is an important co-factor of all biological enzymes, but if the concentration exceeds the threshold of maintaining the homeostasis mechanism, copper will lead to cytotoxicity. This death mechanism has been named "Cuproptosis". The mechanism of cuproptosis distinct from all other known mechanisms of regulated cell death, including apoptosis, pyroptosis, necroptosis, and ferroptosis. Copper combine with the lipoylated components of the tricarboxylic acid cycle (TCA), leading to lipoylated protein aggregation and subsequent loss of iron-sulfur cluster proteins, ultimately resulting in protein toxicity stress and cell death. Studies have shown that the necessary factors for cuproptosis include the presence of glutathione, mitochondrial metabolism of galactose and pyruvate, and glutamine metabolism. Targeted regulation of cuproptosis is a potential choice to treat cancer, rheumatoid arthritis, and other diseases. For example, up-regulation of LIPT1 may inhibit the occurrence and development of tumors by destroying TCA in mitochondria and then inducing cuproptosis. MCE supplies a unique collection of 419 cuproptosis-related compounds, all of which act on the targets or signaling pathways related to cuproptosis and may have in inhibitory or activated effect on cuproptosis. MCE Cuproptosis Library is a useful tool for drug research related to cancer, rheumatoid arthritis, and other diseases.

Cuproptosis Compound Library

419 compounds

Copper is an important co-factor of all biological enzymes, but if the concentration exceeds the threshold of maintaining the homeostasis mechanism, copper will lead to cytotoxicity. This death mechanism has been named "Cuproptosis".

The mechanism of cuproptosis distinct from all other known mechanisms of regulated cell death, including apoptosis, pyroptosis, necroptosis, and ferroptosis.

Copper combine with the lipoylated components of the tricarboxylic acid cycle (TCA), leading to lipoylated protein aggregation and subsequent loss of iron-sulfur cluster proteins, ultimately resulting in protein toxicity stress and cell death. Studies have shown that the necessary factors for cuproptosis include the presence of glutathione, mitochondrial metabolism of galactose and pyruvate, and glutamine metabolism.

Targeted regulation of cuproptosis is a potential choice to treat cancer, rheumatoid arthritis, and other diseases. For example, up-regulation of LIPT1 may inhibit the occurrence and development of tumors by destroying TCA in mitochondria and then inducing cuproptosis.

MCE supplies a unique collection of 419 cuproptosis-related compounds, all of which act on the targets or signaling pathways related to cuproptosis and may have in inhibitory or activated effect on cuproptosis. MCE Cuproptosis Library is a useful tool for drug research related to cancer, rheumatoid arthritis, and other diseases.

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-N10319

Artepillin C	Ketones, Aldehydes, Acids Plants Compositae Artemisia capillaris Thunb. Source Classification	Epigenetic Reader Domain Necroptosis TRP Channel
Artepillin C is an orally active CREB/CRTC2 inhibitor and TRPA1 covalent agonist (EC₅₀=1.8 μM). Artepillin C inhibits CREB/CRTC2-mediated gene transcription and downregulates BMAL1 expression to regulate glucose and lipid metabolism. Artepillin C can also activate TRPA1 channels to induce spicy taste signals. Artepillin C can inhibit tumor cell proliferation, induce *necroptosis, improve insulin resistance and inhibit liver lipid synthesis. Artepillin C can be used in the study of metabolic syndrome, tumor* prevention and treatment, and inflammation .

HY-N0660

Jujuboside B	Cardiovascular Disease Triterpenes Structural Classification other families Classification of Application Fields Terpenoids Plants Disease Research Fields Source Classification	Apoptosis PARP Caspase AMPK Autophagy VEGFR Keap1-Nrf2 STING 11β-HSD Ferroptosis PI3K Akt p38 MAPK ERK
Jujuboside B is a bioactive saponin component isolated from Ziziphi Spinosae Semen (sour jujube seed), with oral efficacy and blood-brain barrier permeability. Jujuboside B induces acute leukemia cell death and drives necroptosis apoptosis by activating the RIPK1/RIPK3/MLKL pathway. Jujuboside B upregulates the expression of NOXA, PARP and caspase-3, activates AMPK, inhibits the proliferation of breast cancer cells, and induces cell apoptosis and autophagy. Jujuboside B inhibits angiogenesis and tumor growth by blocking the VEGFR-2 signaling pathway. Jujuboside B alleviates liver injury in mice by regulating the Nrf2-STING signaling pathway . Jujuboside B alleviates liver injury by regulating anti-inflammatory responses and downregulating the expression of 11β-HSD2. Jujuboside B induces ferroptosis and overcomes radioresistance in non-small cell lung cancer via the PPARγ-ATF3-Gpx4 signaling pathway. Jujuboside B exerts inhibitory effects on platelet aggregation. Jujuboside B inhibits febrile seizures by suppressing the activity of AMPA receptors. Jujuboside B reverses chronic unpredictable mild stress-promoted tumor progression by blocking the PI3K/Akt and MAPK/ERK pathways and dephosphorylating CREB signaling. Jujuboside B is applicable to related studies on acute leukemia, breast cancer, PM_2.5-induced lung injury, hepatotoxicity, liver injury, colorectal cancer, non-small cell lung cancer, thromboembolic diseases, cardiovascular diseases associated with high platelet aggregation, febrile seizures, and depressive-like phenotypes .

HY-N0660R

Jujuboside B (Standard)	Triterpenes Structural Classification other families Terpenoids Plants Source Classification	Reference Standards ERK p38 MAPK Akt PI3K 11β-HSD STING VEGFR Ferroptosis Autophagy Apoptosis Keap1-Nrf2 Caspase PARP AMPK
Jujuboside B (Standard) is the analytical standard of Jujuboside B. This product is intended for research and analytical applications. Jujuboside B is a bioactive saponin component isolated from Ziziphi Spinosae Semen (sour jujube seed), with oral efficacy and blood-brain barrier permeability. Jujuboside B induces acute leukemia cell death and drives necroptosis apoptosis by activating the RIPK1/RIPK3/MLKL pathway. Jujuboside B upregulates the expression of NOXA, PARP and caspase-3, activates AMPK, inhibits the proliferation of breast cancer cells, and induces cell apoptosis and autophagy. Jujuboside B inhibits angiogenesis and tumor growth by blocking the VEGFR-2 signaling pathway. Jujuboside B alleviates liver injury in mice by regulating the Nrf2-STING signaling pathway . Jujuboside B alleviates liver injury by regulating anti-inflammatory responses and downregulating the expression of 11β-HSD2. Jujuboside B induces ferroptosis and overcomes radioresistance in non-small cell lung cancer via the PPARγ-ATF3-Gpx4 signaling pathway. Jujuboside B exerts inhibitory effects on platelet aggregation. Jujuboside B inhibits febrile seizures by suppressing the activity of AMPA receptors. Jujuboside B reverses chronic unpredictable mild stress-promoted tumor progression by blocking the PI3K/Akt and MAPK/ERK pathways and dephosphorylating CREB signaling. Jujuboside B is applicable to related studies on acute leukemia, breast cancer, PM_2.5-induced lung injury, hepatotoxicity, liver injury, colorectal cancer, non-small cell lung cancer, thromboembolic diseases, cardiovascular diseases associated with high platelet aggregation, febrile seizures, and depressive-like phenotypes.

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