VEGFR Inhibitor

Icrucumab (Anti-VEGFR1/FLT1 Reference Antibody; IMC-18F1) is an IgG1 antibody inhibitor targeting VEGFR-1/FLT1 with anti-tumor activity. By blocking ligand-dependent phosphorylation and downstream signal transduction, Icrucumab reduces the activities of MAPK and Akt in breast cancer xenograft models, inhibits the proliferation and invasion of VEGFR-1-positive tumor cells, and reverses the conversion of M1 macrophages to the pro-tumor M2-like phenotype. Icrucumab also inhibits tumor cell proliferation, promotes apoptosis, and effectively suppresses tumor growth through direct targeting of tumors and host support mechanisms. In addition, Icrucumab exhibits a synergistic effect when combined with chemotherapeutic agents, and it is used in research related to various cancers including advanced solid malignancies, thyroid cancer, melanoma, and lung cancer.

SSGJ-707 (PF-08634404) is a bispecific antibody targeting VEGF and PD-1. SSGJ-707 exerts dual anti-tumor effects by neutralizing VEGF and blocking the PD-1 signaling pathway. SSGJ-707 can be combined with platinum-based chemotherapy to inhibit advanced non-small cell lung cancer (NSCLC), and its inhibitory effect is not limited by PD-L1 expression levels. In the HARMONi-2 trial, the objective response rate of SSGJ-707 correlates with the PD-L1 tumor proportion score, and the incidence of grade ≥3 adverse events is comparable to that of Inetetamab (HY-P99969). SSGJ-707 is being extensively investigated for a variety of malignancies including advanced NSCLC, colorectal cancer and small cell lung cancer.

Raddeanin A is an oleanane-type triterpenoid saponin with oral activity. Raddeanin A inhibits SRC, mTOR, JNK, VEGFR2, NLRP3 inflammasome, Wnt/β-catenin, Wee1, PI3K/AKT signaling pathway, MAPK/ERK signaling pathway, AR-FL, AR-Vs, and downregulates the expression of p-PI3K and p-AKT. Raddeanin A inhibits osteoclast formation, bone resorption, osteolysis, cancer cell invasion, migration, proliferation, angiogenesis and epithelial-mesenchymal transition, while induces apoptosis, cell cycle arrest, ROS production, immunogenic cell death and dendritic cell maturation. Raddeanin A improves blood-retinal barrier function, alleviates inflammation, regulates the tumor microenvironment, and enhances the activity of anti-PD-1 antibody. Raddeanin A is applicable to the research of breast cancer-associated osteolysis, human osteosarcoma, colorectal cancer, glioblastoma, Alzheimer's disease, cholangiocarcinoma, melanoma, non-small cell lung cancer, castration-resistant prostate cancer and multiple myeloma.

Pegaptanib sodium is an RNA aptamer with polyethylene glycol modifications, which is directed against vascular endothelial growth factor (VEGF)-165. Pegaptanib could be used for the study of neovascular age-related macular degeneration (AMD) .

Tyrphostin A9, a PDGFR inhibitor, is a potent inducer of mitochondrial fission. Tyrphostin A9 emerged as the most potent and selective of 51 tyrosine kinase inhibitors tested against the TNF-induced respiratory burst. Tyrphostin A9 has anti-influenza virus activities.

AST 487 is a RET kinase inhibitor with IC₅₀ of 880 nM, inhibits RET autophosphorylation and activation of downstream effectors, also inhibits Flt-3 with IC₅₀ of 520 nM.

SU11652 is a potent receptor tyrosine kinase (RTK) inhibitor. SU11652 also inhibits several members of the split kinase family of RTKs, including VEGFR, FGFR, PDGFR, and Kit. SU11652 can be uesd for spontaneous cancers expressing Kit mutations research.

Ethyl cinnamate, an orally active chemical constituent of the rhizome of Kaempferia galanga, exhibits anti-cancer, nematocidal, sedative and vasorelaxant activities. Ethyl cinnamate is a fragrance ingredient used as a food flavor and additive for cosmetic products. Ethyl cinnamate is also an excellent clearing reagent for mammalian tissues. Ethyl cinnamate suppresses tumor growth through anti-angiogenesis by attenuating VEGFR2 signal pathway in colorectal cancer. Ethyl cinnamate inhibits the tonic contractions induced by high K+ and phenylephrine (PE) with respective IC₅₀ values of 0.30 mM and 0.38 mM in rat aorta.

AMG-47a is an orally active, ATP-competitive Lck inhibitor (IC₅₀=0.2 nM). AMG-47a inhibits VEGF2, p38α, p38α, Jak3, MLR, and IL-2 with IC₅₀ of 1 nM, 3 nM, 72 nM, 30 nM, and 21 nM, respectively. AMG-47a reduces T cell activation and the production of cytokines such as TGF-β, exerting anti-inflammatory and anti-fibrotic activities. AMG-47a can be used in the research of autoimmune diseases, pulmonary fibrosis, and KRAS mutation-associated cancers[1][2][3].

Ki20227 is an orally active and highly selective c-Fms tyrosine kinase (CSF1R) inhibitor with IC₅₀s of 2 nM, 12 nM, 451 and 217 nM for CSF1R, VEGFR2 (vascular endothelial growth factor receptor-2), c-Kit (stem cell factor receptor) and PDGFRβ (platelet-derived growth factor receptor β). Ki20227 suppresses osteoclast differentiation and osteolytic bone destruction.

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.

Mollugin is an orally active and potent NF-κB inhibitor. Mollugin induces S-phase arrest of HepG2 cells, and increased intracellular reactive oxygen species (ROS) levels. Mollugin induces DNA damage in HepG2 cells, as well as an increase in the expression of p-H2AX. Mollugin shows anti-cancer effect by inhibiting TNF-α-induced NF-κB activation. Mollugin enhances the osteogenic action of BMP-2 (bone morphogenetic protein 2) via the p38-Smad signaling pathway.

Chloramphenicol (Standard) is the analytical standard of Chloramphenicol. This product is intended for research and analytical applications. Chloramphenicol is an orally active, potent and broad-spectrum antibiotic. Chloramphenicol shows antibacterial activity. Chloramphenicol represses the oxygen-labile transcription factor and hypoxia inducible factor-1 alpha (HIF-1α) in hypoxic A549 and H1299 cells. Chloramphenicol suppresses the mRNA levels of vascular endothelial growth factor (VEGF) and glucose transporter 1, eventually decreasing VEGF release. Chloramphenicol can be used for anaerobic infections and lung cancer research.

6'-Sialyllactose promotes the growth of beneficial bacteria (such as Bifidobacterium and lactobacillus) and inhibits the proliferation of harmful bacteria. 6'-Sialyllactose exhibits anti-inflammatory and anti-angiogenic activities. 6'-Sialyllactose promotes the muscle health.

Glycine (Standard) is the analytical standard of Glycine. This product is intended for research and analytical applications. Glycine is an inhibitory neurotransmitter in the CNS and also acts as a co-agonist along with glutamate, facilitating an excitatory potential at the glutaminergic N-methyl-D-aspartic acid (NMDA) receptors. Glycine is orally active. Glycine can be used to study cell protection, cancer, neurological diseases, and angiogenesis.

BIBF 1202 is the carboxylate metabolite of Nintedanib (HY-50904) which inhibits VEGFR2 kinase with an IC₅₀ of 62 nM.

ST6GAL1-IN-1 is an orally active selective ST6GAL1 inhibitor (IC₅₀ = 20 μM). ST6GAL1-IN-1 exhibits high antimetastatic potential, effectively inhibiting the migration of MDA-MB-231 cells at noncytotoxic concentrations. ST6GAL1-IN-1 can disrupt integrin sialylation in MDA-MB-231 cells. ST6GAL1-IN-1 inhibits tumor angiogenesis and cancer metastasis via the Integrin/VEGFR2-mediated signaling pathway. ST6GAL1-IN-1 effectively suppresses both tumor growth and cancer metastasis on the MDA-MB-231 xenograft model. ST6GAL1-IN-1 can be used for the study of Triple-negative breast cancer (TNBC).

5-O-Methylvisammioside (4'-O-β-D-Glucosyl-5-O-methylvisamminol) is an orally active natural chromone glycoside and multiple biological activities. 5-O-Methylvisammioside inhibits ferroptosis by activating the Nrf2/HO-1 signaling axis. 5-O-Methylvisammioside alleviates intestinal barrier damage by inhibiting the ROS/NF-κB/NLRP3 pathway. 5-O-Methylvisammioside exerts a protective effect against acute liver injury by reducing ALT/AST, decreasing inflammatory infiltration, and inhibiting IκB-α phosphorylation and NF-κB nuclear translocation. 5-O-Methylvisammioside blocks the HMGB1/RAGE/MEK/ERK signaling axis to exert anti-tumor and anti-angiogenic effects. 5-O-Methylvisammioside improves depression-like behaviors by inhibiting Src kinase and the NF-κB pathway.

Brolucizumab (DLX1008) is a single-chain anti-VEGF-A antibody fragment with low picomolar affinity (K_D=1.05 pM). Brolucizumab can be used for the research of cancer.

ATWLPPR Peptide is a biological active peptide. (This peptide is a specific VEGFR2/KDR heptapeptide antagonist, it binds VEGFR2 (KDR/flk), completely inhibiting VEGF binding to KDR and preventing VEGF-induced angiogenesis in-vivo. It specifically inhibits human endothelial cell proliferation in-vitro and totally abolishes VEGF-induced angiogenesis in-vivo.)