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Abietic acid, an orally active diterpene isolated from Colophony, displays significant anti-proliferative, anti-inflammatory, anti-obesity effect, bacteriostatic, cell cycle arresting and pro-apoptotic activities. Abietic acid inhibits lipoxygenase activity for allergy. Abietic acid enhances cell migration and tube formation in HUVECs. Abietic acid induces significant angiogenic potential, which is associated with upregulation of extracellular signal-regulated kinase (ERK) and p38 expression. Abietic acid attenuates sepsis-induced lung injury by inhibiting nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway to inhibit M1 macrophage polarization. Abietic acid exhibits a positive effect against liver injury by attenuating inflammation and ferroptosis. Abietic acid shows accelerated wound closure in a mouse model of cutaneous wounds. Abietic acid significantly reduces the proliferation and growth of NSCLC cells by IKKβ inhibition.Additionally, Abietic acid ameliorates psoriasis-like inflammation and modulates gut microbiota in mice. Abietic acid is promising for research in non-small-cell lung cancer (NSCLC), liver injury-related deseases and psoriasis .
WRW4, a specific formyl peptide receptor-like 1 (FPRL1) antagonist, inhibits WKYMVm binding to FPRL1 with an IC50 of 0.23 μM. WRW4 specifically inhibits the increase in intracellular calcium by the FPRL1 agonists MMK-1, amyloid beta42 (Abeta42) peptide, and F peptide .
Resolvin D1 (RvD1), an endogenous pro-resolving mediator of inflammation, is derived from omega-3 docosahexaenoic acid during the resolution phase of acute inflammation. Resolvin D1 blocks proinflammatory neutrophil migration by regulating actin polymerization, reduces TNF-α–mediated inflammation in macrophages, and enhances phagocytosis of apoptotic cells by macrophages .
Iguratimod is an antirheumatic agent, acts as an inhibitor of COX-2, with an IC50 of 20 μM (7.7 μg/mL), but shows no effect on COX-1. Iguratimod also inhibits macrophagemigration inhibitory factor (MIF) with an IC50 of 6.81 μM.
TRAF-STOP inhibitor 6877002 is a selective CD40-TRAF6 interaction inhibitor. TRAF-STOP inhibitor 6877002 exerts anti-atherosclerotic activity by blocking the CD40-TRAF6 signaling pathway, inhibiting classical monocyte activation, leukocyte recruitment, and macrophage activation and migration. TRAF-STOP inhibitor 6877002 reduces the phosphorylation levels of signaling intermediates in the canonical NF-κB pathway .
Darutoside is an orally effective diterpene compound with significant anti-inflammatory, analgesic, wound healing promotion, and immunomodulatory activities. Darutoside reduces edema and pain responses by inhibiting the expression of COX-2 and the migration of inflammatory cells. It regulates macrophage polarization towards the M2 type by inhibiting the NF-κB pathway, alleviating inflammation and promoting wound healing. Through multi-target regulation of metabolic networks, Darutoside significantly alleviates acute gouty arthritis .
Kumatakenin is an orally active apoptosis inducer and autophagy inhibitor, with a Kd value of 2.94 μM for mouse ATG5. Kumatakenin increases the activities of caspase-3, caspase-8 and caspase-9, thereby inducing caspase-dependent apoptosis in ovarian cancer cells. Kumatakenin reduces the expression of chemokines and pro-oncogenic factors in ovarian cancer cells, and inhibits M2 macrophage polarization. Kumatakenin inactivates TRIM65 function, reduces the expression and stability of FASN, and thus inhibits the proliferation, migration, invasion and tumor progression of esophageal cancer cells. Kumatakenin interacts with ATG5 to reduce its protein level, decrease LC3 level, and reduce the number of autophagosomes in the hippocampus. Kumatakenin binds to Eno3 to upregulate its expression, reduce the stability and expression level of IRP1 mRNA, inhibit ferroptosis, alleviate intestinal inflammation, and restore epithelial barrier function. Kumatakenin enhances the efficacy of antibiotics against pathogenic bacteria, inhibits SARS-CoV-2 replication, and reduces cytokine production. Kumatakenin is applicable to research related to ovarian cancer, esophageal cancer, depression and colitis .
MIF098 is a macrophagemigration inhibitory factor (MIF) antagonist. MIF098 inhibits proliferation, migration and fibrosis of pulmonary smooth muscle cells. MIF098 can be used for immunoinflammation-related disease research .
Neopterin is an immune system activator metabolized by GTP and can be produced by activated macrophages. Neopterin has the potential to resist vascular inflammation and atherosclerosis. Neopterin inhibits the phosphorylation of NF-κB and promotes the expression of PPAR-γ, thereby suppressing the inflammatory response of vascular endothelial cells, reducing the formation of macrophage foam cells, and regulating the migration and proliferation of vascular smooth muscle cells. Neopterin can be used in research fields such as cardiovascular diseases (such as atherosclerosis), inflammation-related diseases and tumor immunomonitoring .
(E)-Osmundacetone is an inhibitor of the MAPK pathway. (E)-Osmundacetone inhibits the activation of the MAPK signaling pathway and restores the expression of PPARα/ACOX1. (E)-Osmundacetone abrogates abnormal cell proliferation, migration and liver metastasis induced by PTPRO silencing in colorectal cancer cells. (E)-Osmundacetone blocks OA-RD17-mediated activation of the MAPK signaling pathway, thereby reducing macrophage proliferation and migration. (E)-Osmundacetone is applicable to relevant research on colorectal cancer .
TRPV2-selective blocker 1 is a TRPV2-selective blocker that inhibits calcium influx and ionic currents. TRPV2-selective blocker 1 exhibits an IC50 of 6.3 μM against rat TRPV2, and shows no activity against TRPV1, TRPV3 or TRPV4 channels. TRPV2-selective blocker 1 attenuates macrophage phagocytosis, LPS-induced macrophagemigration, and calcium microdomains generated by peripheral TRPV2. TRPV2-selective blocker 1 is non-cytotoxic and can be used to investigate the function of TRPV2 during immune processes .
Anti-CD47 Antibody (B6.H12) is a kind of mouse IgG1 κ chimeric antibody, targeting to human CD47. Anti-CD47 Antibody (B6.H12) blocks CD47 interactions with SIRPα. Anti-CD47 Antibody (B6.H12) inhibits cell proliferation, cell migration and invasion. Anti-CD47 Antibody (B6.H12) increases macrophage phagocytosis. Anti-CD47 Antibody (B6.H12) shows potent anti-tumor effect in various tumor models, such as osteosarcoma .
Lotus tetragonolobus lectin (LTL) is a plant lectin that specifically recognizes and binds to α-L-fucopyranosyl residues, a sugar structure serving as the key terminal glycosyl group of human blood type O antigen (H antigen). Lotus tetragonolobus lectin exerts macrophagemigration inhibitory activity in monomeric form. Lotus tetragonolobus lectin labels and identifies renal proximal tubular epithelial cells to evaluate histopathological changes of sepsis-induced acute kidney injury. Lotus tetragonolobus lectin is applicable to studies in glycobiology, immunology and renal pathology .
TL-895 is a potent, orally active, ATP-competitive, and highly selective irreversible BTK inhibitor. TL-895 is active against recombinant BTK (average IC50: 1.5 nM) and inhibits only three additional kinases BLK, BMX (IC50 = 1.6 nM) and TXK with IC50 within tenfold of BTK activity. TL-895 inhibits BTK auto-phosphorylation at the Y223 phosphorylation site (IC50: 1-10 nM). The TL-895 effectively inhibits the production of inflammatory factors such as IL-8, IL-1β, MCP-1 and TNF-α by monocytes or macrophages, and reduces the chemotactic migration of MF cells towards SDF-1. TL-895 is used be for studies of chronic lymphocytic leukemia (CLL), myelofibrosis (MF), and B-cell malignancies .
BTZO-1, a chemical probe, binds to Macrophagemigration inhibitory factor (MIF) with a Kd value of 68.6 nM, and its binding requires the N-terminal Pro1. BTZO-1 can activate antioxidant response element (ARE)-mediated gene expression and suppress oxidative stress-induced cardiomyocyte apoptosis in vitro .
3-Cyanoumbelliferone is a coumarin derivative, acting as molecular probe and fluorescent dye. 3-Cyanoumbelliferone is also a macrophagemigration inhibitory factor (MIF) tautomerase inhibitor with a Ki of 2.9 μM .
Exoenzyme C3, clostridium botulinum, is a mono-ADP-ribosylating enzyme. Exoenzyme C3, clostridium botulinum specifically modifies RhoA, B, and C by transferring ADP-ribose to them, thereby inactivating these GTPases. Exoenzyme C3, clostridium botulinum can induce neuronal axonal and dendritic growth, inhibit macrophagemigration, and regulate cytoskeletal dynamics. Exoenzyme C3, clostridium botulinum can be used in the research of spinal cord injury and diabetic painful neuropathy .
DT-6 is an effective TGF-β1 inhibitor. DT-6 inhibits M2 macrophage induced epithelial to mesenchymal transition and invasive migration of cancer cells. DT-6 can be used for cancer diseases research .
Resolvin D1-d5 is the deuterium labeled Resolvin D1. Resolvin D1 (RvD1), an endogenous pro-resolving mediator of inflammation, is derived from omega-3 docosahexaenoic acid during the resolution phase of acute inflammation. Resolvin D1 blocks proinflammatory neutrophil migration by regulating actin polymerization, reduces TNF-α-mediated inflammation in macrophages, and enhances phagocytosis of apoptotic cells by macrophages .
CCR4 antagonist 3 is a potent chemokine receptor 4 (CCR4) antagonist with an IC50 value of 1.7 μM for [ 125I]TARC (thymus and activation regulated chemokine). CCR4 antagonist 3 inhibits binding of radiolabeled TARC and macrophage-derived chemokine (MDC) to CCR4 receptors on the surface of CEM cells. CCR4 antagonist 3 also inhibits the in vitromigration of CEM cells mediated by TARC (IC50 = 6.4 μM) .
Sudachitin is an orally active compound that potently inhibits mouse PDE1C and human PDE4B, with IC50 values of 5.0 μM and 15.0 μM, respectively. Sudachitin upregulates Sirt1 and PGC‑1α expression in skeletal muscle to regulate energy metabolism and promote mitochondrial biogenesis. Sudachitin improves lipid metabolism, glucose tolerance, insulin sensitivity, energy expenditure, and fatty acid β‑oxidation. Sudachitin activates p38MAPK signaling, induces HSP27 phosphorylation and caspase‑dependent apoptosis, and blocks EGF‑driven keratinocyte migration and proliferation. Sudachitin suppresses LPS‑induced TNF‑α, NO, and iNOS expression in macrophages and shows potent anti‑inflammatory activity. Sudachitin can be used for the research of metabolic syndrome, type 2 diabetes, and psoriasis. .
CSF1R-IN-3 (compound 21) is a potent and orally active CSF-1R inhibitor (IC50=2.1 nM). CSF1R-IN-3 is a potent antiproliferative activity against colorectal cancer cells. CSF1R-IN-3 inhibits the progression of colorectal cancer by suppressing the migration of macrophages, reprograming M2-like macrophages to the M1 phenotype, and enhancing the antitumor immunity .
ISO-1 (Standard) is the analytical standard of ISO-1. This product is intended for research and analytical applications. ISO-1 is a macrophagemigration inhibitory factor (MIF) antagonist with an IC50 of 7 μM.
MIF-IN-4 hydrochloride is potent macrophagemigration inhibitory factor (MIF) inhibitor (pIC50=5.01-6). MIF is a cytokine originally found to play a role in inhibiting macrophagemigration .
MIF-IN-5 (compound 1d) is a potent and reversible macrophagemigration inhibitory factor (MIF) competitive inhibitor with an IC50 of 4.8 μM and a Ki value of 3.3 μM, respectively .
MIF-IN-6 (compound 2d) is a potent macrophagemigration inhibitory factor (MIF) inhibitor with an IC50 of 1.4 μM and a Ki value of 0.96 μM, respectively. MIF-IN-6 attenuates MIF-induced ERK phosphorylation and inhibits proliferation of A549 cells .
Carebastine-d5 is the deuterium labeled Carebastine. Carebastine is the active metabolite of Ebastine. Carebastine is a histamine H1 receptor antagonist. Carebastine inhibits VEGF-induced HUVEC and HPAEC proliferation, migration and angiogenesis in a dose-dependent manner . Carebastine suppresses the expression of macrophagemigration inhibitory factor .
R110 is a potent, competitive inhibitor of macrophagemigration inhibitory factor 2 (MIF2) tautomerase with an IC50 of 15 μM. R110 has the potential for the research of cancer diseases .
Carebastine-d5 Methyl Ester is the deuterium labeled Carebastine. Carebastine is the active metabolite of Ebastine. Carebastine is a histamine H1 receptor antagonist. Carebastine inhibits VEGF-induced HUVEC and HPAEC proliferation, migration and angiogenesis in a dose-dependent manner . Carebastine suppresses the expression of macrophagemigration inhibitory factor .
HTS05585 (Compound Hit-1) is a selective macrophagemigration inhibitory factor (MIF) inhibitor with a Kd value of 0.29 μM measured by microscale thermophoresis (MST) and 0.32±0.01 μM verified by isothermal titration calorimetry (ITC). HTS05585 inhibits the release of pro-inflammatory factors (TNF-α, IL-6, IL-1β) from LPS-induced macrophages. HTS05585 is promising for research of inflammation-related diseases such as sepsis .
Iguratimod (Standard) is the analytical standard of Iguratimod. This product is intended for research and analytical applications. Iguratimod is an antirheumatic agent, acts as an inhibitor of COX-2, with an IC50 of 20 μM (7.7 μg/mL), but shows no effect on COX-1. Iguratimod also inhibits macrophagemigration inhibitory factor (MIF) with an IC50 of 6.81 μM.
(E)-Osmundacetone (Standard) is the analytical standard of (E)-Osmundacetone (HY-N1966). This product is intended for research and analytical applications. (E)-Osmundacetone is an inhibitor of the MAPK pathway. (E)-Osmundacetone inhibits the activation of the MAPK signaling pathway and restores the expression of PPARα/ACOX1. (E)-Osmundacetone abrogates abnormal cell proliferation, migration and liver metastasis induced by PTPRO silencing in colorectal cancer cells. (E)-Osmundacetone blocks OA-RD17-mediated activation of the MAPK signaling pathway, thereby reducing macrophage proliferation and migration. (E)-Osmundacetone is applicable to relevant research on colorectal cancer .
PLD-IN-1 (Compound 3r) is an orally active inhibitor for phospholipase D with an IC50 of 1.97 μM. PLD-IN-1 reduces the expression of CD24, CD47 and PD-L1, enhances the calreticulin expression, and thus modulates the immune evasion mechanism in lung cancer cells by promoting the phagocytosis of cancer cells by macrophages. PLD-IN-1 inhibits the cell viability of lung cancer cell A549, HCC44, H460 and HCC15 with IC50 of 18.44, 22.31, 24.85 and 21.45 μM, respectively. PLD-IN-1 can induce apoptosis and inhibits migration in cell A549. PLD-IN-1 enhances the level of pro-inflammatory M1 macrophages and decreases the level of anti-inflammatory M2 macrophages, exhibits antitumor efficacy in mouse model .
PAV-174 is a potent antiviral agent that targets a host protein. PAV-174 prevents Herpes simplex virus (HSV-1) infection in cells (IC50 of 0.02 μM in Vero cells) and human brain organoids. PAV-174 inhibits oxidized macrophagemigration inhibitory factor (oxMIF)-induced tau phosphorylation in vitro and in vivo independent of infection. PAV-174 reduces HSV-1-induced tau phosphorylation via the Akt/GSK3β signaling pathway. PAV-174 can be used for Alzheimer’s disease research .
PAANIB-1 is a parthanatos associated apoptosis-inducing factor nuclease (PAAN)/macrophagemigration inhibitor factor (MIF) inhibitor. PAANIB-1 exhibits neuroprotective activity. PAANIB-1 can be used for the research of Parkinson's disease .
HE4-1 leech peptide is a p38 MAPK inhibitor with an additional c-Jun N-terminal kinase (JNK) inhibitory role. HE4-1 leech peptide suppresses macrophagemigration, and does not significantly affect macrophage immunological activities including phagocytic ability, lysozyme activity, and expression levels of most inflammatory factors. HE4-1 leech peptide can be used for the research of atherosclerosis .
IKVAVC is a derivative peptide of IKVAV with an artificially added cysteine (Cys) at its C-terminus. IKVAVC retains all the biological activities of the original IKVAV, mainly acting as a neural adhesion/differentiation signaling peptide, and is equipped with an engineered linker arm that enables covalent conjugation to molecular materials. IKVAV inhibits the migration and activation of fibroblasts, downregulates the TGF-β1 signaling pathway and endoplasmic reticulum stress, and promotes nerve repair. IKVAV regulates the phenotype of macrophages, shifting them from the pro-inflammatory M1 type to the pro-reparative M2 type .
NEO212 is an orally active, blood-brain barrier permeable conjugate of Temozolomide (TMZ) (HY-17364) and Perillyl Alcohol (POH) (HY-N7000), with potent anticancer activity. NEO212 overcomes classical TMZ resistance and DNA alkylation by depleting MGMT. By inhibiting the FAK/Src signaling pathway, NEO212 reduces the production of MMP2 and MMP9, induces mesenchymal-epithelial transition, and inhibits the migration, invasion and tumor progression of glioma stem cells. NEO212 disrupts autophagy flux to enhance mitochondrial apoptosis; it induces differentiation of acute myeloid leukemia (AML) cells into macrophages and proliferation arrest .
CT-133 is a selective and potent CRTH2 Receptor antagonist, with a Ki value of 2.2 nM. The Ki value for the DP1 receptor is greater than 3800 nM. CT-133 inhibits neutrophil migration induced by PGD2 (HY-101988). CT-133 significantly alleviates lung inflammation and improves lung function impairment in a mouse model of acute lung injury (ALI) induced by cigarette smoke. CT-133 effectively inhibits the excessive expression of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) and chemokines (KC), and reverses the inhibition of the anti-inflammatory factor IL-10. CT-133 can be used for the study of ALI .
EED-IN-5 is an orally active, EZH2-selective trisubstituted pyridine-based EED-H3K27me3 inhibitor and immunomodulator with anti-inflammatory activity. The IC50 value of EED-IN-5 against EED is 28.21 nM. In mouse models, EED-IN-5 preferentially and persistently accumulates in lymph nodes after oral administration. By reducing the H3K27me3 level of dendritic cells and inhibiting their migration, EED-IN-5 decreases the infiltration of specific dendritic cells, macrophages and T cells into the spinal cord and brain. EED-IN-5 exhibits hERG inhibitory activity, shows negative results in the Mini-Ames test, and causes no obvious toxicity upon long-term high-dose administration. EED-IN-5 can be used for the research of multiple sclerosis .
D-DT/MIF-1-IN-1 (Compound 4h) is a non-competitive, non-covalent inhibitor of MIF-1 and D-DT, with IC50 values of 2.4 μM and 4.0 μM against D-DT, and an IC50 value of 9.8 μM against MIF-1. D-DT/MIF-1-IN-1 inhibits D-DT-induced phosphorylation of ERK and exerts antiproliferative activity in non-small cell lung cancer cells .
Lotus tetragonolobus lectin (LTL) is a plant lectin that specifically recognizes and binds to α-L-fucopyranosyl residues, a sugar structure serving as the key terminal glycosyl group of human blood type O antigen (H antigen). Lotus tetragonolobus lectin exerts macrophagemigration inhibitory activity in monomeric form. Lotus tetragonolobus lectin labels and identifies renal proximal tubular epithelial cells to evaluate histopathological changes of sepsis-induced acute kidney injury. Lotus tetragonolobus lectin is applicable to studies in glycobiology, immunology and renal pathology .
WRW4, a specific formyl peptide receptor-like 1 (FPRL1) antagonist, inhibits WKYMVm binding to FPRL1 with an IC50 of 0.23 μM. WRW4 specifically inhibits the increase in intracellular calcium by the FPRL1 agonists MMK-1, amyloid beta42 (Abeta42) peptide, and F peptide .
HE4-1 leech peptide is a p38 MAPK inhibitor with an additional c-Jun N-terminal kinase (JNK) inhibitory role. HE4-1 leech peptide suppresses macrophagemigration, and does not significantly affect macrophage immunological activities including phagocytic ability, lysozyme activity, and expression levels of most inflammatory factors. HE4-1 leech peptide can be used for the research of atherosclerosis .
IKVAVC is a derivative peptide of IKVAV with an artificially added cysteine (Cys) at its C-terminus. IKVAVC retains all the biological activities of the original IKVAV, mainly acting as a neural adhesion/differentiation signaling peptide, and is equipped with an engineered linker arm that enables covalent conjugation to molecular materials. IKVAV inhibits the migration and activation of fibroblasts, downregulates the TGF-β1 signaling pathway and endoplasmic reticulum stress, and promotes nerve repair. IKVAV regulates the phenotype of macrophages, shifting them from the pro-inflammatory M1 type to the pro-reparative M2 type .
Anti-CD47 Antibody (B6.H12) is a kind of mouse IgG1 κ chimeric antibody, targeting to human CD47. Anti-CD47 Antibody (B6.H12) blocks CD47 interactions with SIRPα. Anti-CD47 Antibody (B6.H12) inhibits cell proliferation, cell migration and invasion. Anti-CD47 Antibody (B6.H12) increases macrophage phagocytosis. Anti-CD47 Antibody (B6.H12) shows potent anti-tumor effect in various tumor models, such as osteosarcoma .
Abietic acid, an orally active diterpene isolated from Colophony, displays significant anti-proliferative, anti-inflammatory, anti-obesity effect, bacteriostatic, cell cycle arresting and pro-apoptotic activities. Abietic acid inhibits lipoxygenase activity for allergy. Abietic acid enhances cell migration and tube formation in HUVECs. Abietic acid induces significant angiogenic potential, which is associated with upregulation of extracellular signal-regulated kinase (ERK) and p38 expression. Abietic acid attenuates sepsis-induced lung injury by inhibiting nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway to inhibit M1 macrophage polarization. Abietic acid exhibits a positive effect against liver injury by attenuating inflammation and ferroptosis. Abietic acid shows accelerated wound closure in a mouse model of cutaneous wounds. Abietic acid significantly reduces the proliferation and growth of NSCLC cells by IKKβ inhibition.Additionally, Abietic acid ameliorates psoriasis-like inflammation and modulates gut microbiota in mice. Abietic acid is promising for research in non-small-cell lung cancer (NSCLC), liver injury-related deseases and psoriasis .
Resolvin D1 (RvD1), an endogenous pro-resolving mediator of inflammation, is derived from omega-3 docosahexaenoic acid during the resolution phase of acute inflammation. Resolvin D1 blocks proinflammatory neutrophil migration by regulating actin polymerization, reduces TNF-α–mediated inflammation in macrophages, and enhances phagocytosis of apoptotic cells by macrophages .
Darutoside is an orally effective diterpene compound with significant anti-inflammatory, analgesic, wound healing promotion, and immunomodulatory activities. Darutoside reduces edema and pain responses by inhibiting the expression of COX-2 and the migration of inflammatory cells. It regulates macrophage polarization towards the M2 type by inhibiting the NF-κB pathway, alleviating inflammation and promoting wound healing. Through multi-target regulation of metabolic networks, Darutoside significantly alleviates acute gouty arthritis .
Kumatakenin is an orally active apoptosis inducer and autophagy inhibitor, with a Kd value of 2.94 μM for mouse ATG5. Kumatakenin increases the activities of caspase-3, caspase-8 and caspase-9, thereby inducing caspase-dependent apoptosis in ovarian cancer cells. Kumatakenin reduces the expression of chemokines and pro-oncogenic factors in ovarian cancer cells, and inhibits M2 macrophage polarization. Kumatakenin inactivates TRIM65 function, reduces the expression and stability of FASN, and thus inhibits the proliferation, migration, invasion and tumor progression of esophageal cancer cells. Kumatakenin interacts with ATG5 to reduce its protein level, decrease LC3 level, and reduce the number of autophagosomes in the hippocampus. Kumatakenin binds to Eno3 to upregulate its expression, reduce the stability and expression level of IRP1 mRNA, inhibit ferroptosis, alleviate intestinal inflammation, and restore epithelial barrier function. Kumatakenin enhances the efficacy of antibiotics against pathogenic bacteria, inhibits SARS-CoV-2 replication, and reduces cytokine production. Kumatakenin is applicable to research related to ovarian cancer, esophageal cancer, depression and colitis .
Neopterin is an immune system activator metabolized by GTP and can be produced by activated macrophages. Neopterin has the potential to resist vascular inflammation and atherosclerosis. Neopterin inhibits the phosphorylation of NF-κB and promotes the expression of PPAR-γ, thereby suppressing the inflammatory response of vascular endothelial cells, reducing the formation of macrophage foam cells, and regulating the migration and proliferation of vascular smooth muscle cells. Neopterin can be used in research fields such as cardiovascular diseases (such as atherosclerosis), inflammation-related diseases and tumor immunomonitoring .
(E)-Osmundacetone is an inhibitor of the MAPK pathway. (E)-Osmundacetone inhibits the activation of the MAPK signaling pathway and restores the expression of PPARα/ACOX1. (E)-Osmundacetone abrogates abnormal cell proliferation, migration and liver metastasis induced by PTPRO silencing in colorectal cancer cells. (E)-Osmundacetone blocks OA-RD17-mediated activation of the MAPK signaling pathway, thereby reducing macrophage proliferation and migration. (E)-Osmundacetone is applicable to relevant research on colorectal cancer .
Sudachitin is an orally active compound that potently inhibits mouse PDE1C and human PDE4B, with IC50 values of 5.0 μM and 15.0 μM, respectively. Sudachitin upregulates Sirt1 and PGC‑1α expression in skeletal muscle to regulate energy metabolism and promote mitochondrial biogenesis. Sudachitin improves lipid metabolism, glucose tolerance, insulin sensitivity, energy expenditure, and fatty acid β‑oxidation. Sudachitin activates p38MAPK signaling, induces HSP27 phosphorylation and caspase‑dependent apoptosis, and blocks EGF‑driven keratinocyte migration and proliferation. Sudachitin suppresses LPS‑induced TNF‑α, NO, and iNOS expression in macrophages and shows potent anti‑inflammatory activity. Sudachitin can be used for the research of metabolic syndrome, type 2 diabetes, and psoriasis. .
(E)-Osmundacetone (Standard) is the analytical standard of (E)-Osmundacetone (HY-N1966). This product is intended for research and analytical applications. (E)-Osmundacetone is an inhibitor of the MAPK pathway. (E)-Osmundacetone inhibits the activation of the MAPK signaling pathway and restores the expression of PPARα/ACOX1. (E)-Osmundacetone abrogates abnormal cell proliferation, migration and liver metastasis induced by PTPRO silencing in colorectal cancer cells. (E)-Osmundacetone blocks OA-RD17-mediated activation of the MAPK signaling pathway, thereby reducing macrophage proliferation and migration. (E)-Osmundacetone is applicable to relevant research on colorectal cancer .
The MIF protein is a pro-inflammatory cytokine that is critical for the innate immune response against bacterial pathogens. Its presence at sites of inflammation suggests a role in modulating macrophage function to promote host defense. MIF Protein, Human (His) is the recombinant human-derived MIF protein, expressed by E. coli , with N-6*His labeled tag.
The MIF protein is a pro-inflammatory cytokine that is critical for the innate immune response against bacterial pathogens. Its presence at sites of inflammation suggests a role in modulating macrophage function to promote host defense. MIF Protein, Human (His) MIF Protein, Human (His, solution) is the recombinant human-derived MIF protein, expressed by E. coli , with N-6*His labeled tag.
The MIF protein is a pro-inflammatory cytokine that is critical for the innate immune response against bacterial pathogens. Its presence at sites of inflammation suggests a role in modulating macrophage function to promote host defense. Animal-Free MIF Protein, Human (His) is the recombinant human-derived animal-FreeMIF protein, expressed by E. coli , with C-His labeled tag. This product is for cell culture use only.
The MIF protein is a pro-inflammatory cytokine that plays a crucial role in the innate immune response against bacterial pathogens.Its presence at sites of inflammation suggests its role as a mediator in the regulation of macrophage function during host defense.MIF Protein, Mouse (His) is the recombinant mouse-derived MIF protein, expressed by E.coli , with C-6*His labeled tag.
The MIF protein is a pro-inflammatory cytokine that plays a crucial role in the innate immune response against bacterial pathogens.Its presence at sites of inflammation suggests its role as a mediator in the regulation of macrophage function during host defense.Animal-Free MIF Protein, Mouse (His) is the recombinant mouse-derived animal-FreeMIF protein, expressed by E.coli , with C-His labeled tag.This product is for cell culture use only.
The MIF protein is a pro-inflammatory cytokine that is critical for the innate immune response against bacterial pathogens. Its presence at sites of inflammation suggests a role in modulating macrophage function to promote host defense. MIF Protein, Human (HEK293, hFc) is the recombinant human-derived MIF protein, expressed by HEK293 , with C-hFc labeled tag.
The MIF protein is a pro-inflammatory cytokine that plays a crucial role in the innate immune response against bacterial pathogens.Its presence at sites of inflammation suggests its role as a mediator in the regulation of macrophage function during host defense.MIF Protein, Mouse (P.pastoris, His) is the recombinant mouse-derived MIF protein, expressed by P.pastoris , with N-6*His labeled tag.
The MIF protein is a pro-inflammatory cytokine that is critical for the innate immune response against bacterial pathogens. Its presence at sites of inflammation suggests a role in modulating macrophage function to promote host defense. MIF Protein, Human (N-His, C-Myc) is the recombinant human-derived MIF protein, expressed by E. coli , with C-Myc, N-10*His labeled tag.
Resolvin D1-d5 is the deuterium labeled Resolvin D1. Resolvin D1 (RvD1), an endogenous pro-resolving mediator of inflammation, is derived from omega-3 docosahexaenoic acid during the resolution phase of acute inflammation. Resolvin D1 blocks proinflammatory neutrophil migration by regulating actin polymerization, reduces TNF-α-mediated inflammation in macrophages, and enhances phagocytosis of apoptotic cells by macrophages .
Carebastine-d5 is the deuterium labeled Carebastine. Carebastine is the active metabolite of Ebastine. Carebastine is a histamine H1 receptor antagonist. Carebastine inhibits VEGF-induced HUVEC and HPAEC proliferation, migration and angiogenesis in a dose-dependent manner . Carebastine suppresses the expression of macrophagemigration inhibitory factor .
Carebastine-d5 Methyl Ester is the deuterium labeled Carebastine. Carebastine is the active metabolite of Ebastine. Carebastine is a histamine H1 receptor antagonist. Carebastine inhibits VEGF-induced HUVEC and HPAEC proliferation, migration and angiogenesis in a dose-dependent manner . Carebastine suppresses the expression of macrophagemigration inhibitory factor .
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
MedchemExpress Validation 03
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
MedchemExpress Validation 04
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
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