Necroptosis Inducer

Methyl methanesulfonate is an alkylating agent which transfers methyl groups, and induces DNA damage. Methyl methanesulfonate is a biochemical reagent that can be used as a biological material or organic compound for life science related research.

Z-VAD is an irreversible, broad-spectrum pan-caspase inhibitor that can inhibit a variety of caspases including caspase-3, -6, -7, -8, -9, etc. (with a weaker inhibitory effect on caspase-2). Z-VAD can block apoptosis signaling pathways, induce autophagy and necrosis in tumor cells, and has anti-angiogenic activity. Z-VAD can enhance the sensitivity of breast cancer and lung cancer cells to radiotherapy in vitro and in vivo, and prolong the growth delay of tumor xenograft models. Z-VAD is well tolerated and is mainly used in research related to cancer radiosensitization and cell death pathway regulation.

ADAR1i-124 is an A-to-I RNA editing inhibitor by inhibiting the catalytic activities of both ADAR1p150 and ADAR1p110. ADAR1i-124 activates type I interferon (IFN) and ZBP1 pathways and dose-dependently inhibits viability across different types of cancer cell lines. ADAR1i-124 can induce cells apoptosis and necroptosis. ADAR1i-124 can be used for the research of cancer, such as cutaneous melanoma and ovarian 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.

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.

Glyphosate, a non-selective systemic biocide with broad-spectrum activity, is an herbicidal derivative of the amino acid glycine. Glyphosate inhibits the enzymatic activity of the 5-endopyruvylshikimate 3-phosphate synthase (EPSPS) in the shikimic acid pathway, preventing the synthesis of the aromatic amino acids tyrosine, phenylalanine, and tryptophan. Glyphosate induces oxidative stress, neuroinflammation, and mitochondrial dysfunction, processes that lead to neuronal death by autophagia, necrosis, or apoptosis, as well as the appearance of behavioral and motor disorders.

RIP1/RIP3/MLKL activator 1 (Compound 6i) is a potent anti-glioma agent. RIP1/RIP3/MLKL activator 1 induces necroptosis through RIP1/RIP3/MLKL pathway. RIP1/RIP3/MLKL activator 1 exerts acceptable BBB permeability.

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.

Periplogenin is an orally active cardiac glycoside found in Cortex periplocae. Periplogenin can induce ROS production and necroptosis and cause G0/G1 phase arrest. Periplogenin can inhibit pyroptosis by regulating the NLRP3/Caspase-1/GSDMD signaling. Periplogenin suppresses growth of prostate carcinoma cells by docking to an ATP1A1 protein pocket and forming a hydrogen bond with T804. Periplogenin can be used for the researches of cancer, inflammation and immunology, such as prostate carcinoma, rheumatoid arthritis and psoriasis.

Chlorhexidine is a orally active cationic antimicrobial agent that targets microbial cell membranes. Chlorhexidine binds to cell membrane phospholipids non-specifically, destroys membrane structure and induces leakage of cell contents. Chlorhexidine has broad-spectrum bactericidal activity against both Gram-positive and Gram-negative bacteria. Chlorhexidine can interfere with membrane permeability, cause protein precipitation and energy metabolism disorders, such as rapid inhibition of microbial growth and induction of cell death (necrosis or apoptosis).

Citronellol ((±)-Citronellol) is an orally active inducer of apoptosis. Citronellol can prevent oxidative stress, mitochondrial dysfunction, and apoptosis in the SH-SY5Y cell Parkinson's disease model induced by 6-OHDA by regulating the ROS-NO, MAPK/ERK, and PI3K/Akt signaling pathways. Citronellol can induce necroptosis in human lung cancer cells through the TNF-α pathway and accumulation of ROS. Citronellol can reduce the levels of LC-3 and p62 to regulate the autophagy pathway, inhibit oxidative stress and neuroinflammation, and thus have neuroprotective effects on Parkinson's rats. Citronellol exhibits anti-fungal activity against Trichophyton rubrum by inhibiting ergosterol synthesis.

ALDH1A inhibitor 673A is an ALDH1A inhibitor with IC₅₀s of 246 nM (ALDH1A1), 230 nM (ALDH1A2), 348 nM (ALDH1A3), respectively. ALDH1A inhibitor 673A has little or no inhibitory effect on other ALDH family members. ALDH1A inhibitor 673A induces necroptotic ovarian cancer stem-like cells (CSCs) death. ALDH1A inhibitor 673A induces DNA double stand breaks in cancer cells. ALDH1A inhibitor 673A can be used for the study of ovarian cancer.

Chlorhexidine digluconate (20% in water) is a orally active cationic antimicrobial agent that targets microbial cell membranes. Chlorhexidine digluconate (20% in water) binds to cell membrane phospholipids non-specifically, destroys membrane structure and induces leakage of cell contents. Chlorhexidine digluconate (20% in water) has broad-spectrum bactericidal activity against both Gram-positive and Gram-negative bacteria. Chlorhexidine digluconate (20% in water) can interfere with membrane permeability, cause protein precipitation and energy metabolism disorders, such as rapid inhibition of microbial growth and induction of cell death (necrosis or apoptosis).

β,β-Dimethylacrylalkannin (Arnebin 1) is an orally active FGFR1 inhibitor (IC₅₀=2.5 μM) and the main active component of Lithospermum erythrorhizon. β,β-Dimethylacrylalkannin blocks downstream signaling by binding to the ATP pocket of FGFR1, and regulates the CDK1/Cdc25C pathway and ROS-JNK axis, thereby inducing G2/M phase arrest, necrosis and apoptosis in cancer cells, and inhibiting tumor proliferation. β,β-Dimethylacrylalkannin also acts as a colistin adjuvant to disrupt the cell membrane of Gram-negative bacteria. β,β-Dimethylacrylalkannin exhibits significant tumor-inhibitory effects with no obvious toxicity in PDX models, but chronic exposure to high doses may alter the relative lung/liver weights of rats, while acute exposure to high doses causes responses such as reduced motor activity. β,β-Dimethylacrylalkannin finds wide application in studies related to hepatocellular carcinoma, colorectal cancer, colistin-resistant bacterial infections, hepatitis and psoriasis.

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.

Chlorhexidine dihydrochloride is a orally active cationic antimicrobial agent that targets microbial cell membranes. Chlorhexidine dihydrochloride binds to cell membrane phospholipids non-specifically, destroys membrane structure and induces leakage of cell contents. Chlorhexidine dihydrochloride has broad-spectrum bactericidal activity against both Gram-positive and Gram-negative bacteria. Chlorhexidine dihydrochloride can interfere with membrane permeability, cause protein precipitation and energy metabolism disorders, such as rapid inhibition of microbial growth and induction of cell death (necrosis or apoptosis).

TP4 (Nile tilapia piscidin) is an orally active amphipathic α-helical cationic antimicrobial peptide. TP4 (Nile tilapia piscidin) exerts broad-spectrum bactericidal activity against Gram-positive and Gram-negative bacteria by disrupting cell membrane structures, and also exhibits certain hemolytic activity. TP4 (Nile tilapia piscidin) regulates the innate immune system and enhances the expression of lysozymes, cytokines and antioxidant enzymes to resist bacterial infection. TP4 (Nile tilapia piscidin) also stimulates the proliferation of keratinocytes and fibroblasts, and significantly promotes the healing of wounds infected with MRSA. TP4 (Nile tilapia piscidin) can be used in research related to bacterial infection, peritonitis, wound healing and other fields.

Duocarmycin SA is an orally active antitumor antibiotic with an IC₅₀ of 10 pM. Duocarmycin SA is an extremely potent cytotoxic agent capable of inducing a sequence-selective alkylation of duplex DNA. Duocarmycin SA demonstrates synergistic cytotoxicity against glioblastoma multiforme (GBM) cells treated with proton radiation in vitro.

Glyphosate (Standard) is the analytical standard of Glyphosate. This product is intended for research and analytical applications. Glyphosate is an herbicidal derivative of the amino acid glycine. Glyphosate targets and blocks a plant metabolic pathway not found in animals, the shikimate pathway, required for the synthesis of aromatic amino acids in plants.

Cyclamic acid sodium (Sodium cyclamate) is a commonly used sweetener. Cyclamic acid sodium is toxic to osteoblasts and can inhibit cell proliferation, induce apoptosis and reduce cell mineralization. Cyclamic acid sodium causes focal necrosis of bladder organs in rats in vitro, which can promote bladder cancer, but some studies have shown that low doses of Cyclamic acid sodium have no carcinogenic effect. In addition, Cyclamic acid sodium has no effect on insulin and glucagon secretion induced by arginine.