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Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!2025-02-06
438 Results for "
BAX
" in MedChemExpress (MCE) Product Catalog:
Products (438)
438 Results for "BAX" in MCE Product Catalog:
Cat. No.: HY-N0278A
CAS No.: 90921-11-2
Synonyms: (Rac)-Pulsatilla camphor; (Rac)-Anemonine
Cat. No.: HY-N0392R
CAS No.: 882664-74-6
Cat. No.: HY-N0559R
CAS No.: 52659-56-0
Cat. No.: HY-173309
Research Areas:
P53/TLR2 modulator-1 (Compound Z9) is a modulator that targets both the P53 pathway and TLR2 simultaneously, exhibiting anti-radiation activity. P53/TLR2 modulator-1 reduces apoptosis by inhibiting the radiation-induced expression of P53 and Bax. At the same time, it activates the TLR2 pathway, upregulates the expression of downstream proteins MyD88 and P65, and promotes the secretion of cytokines such as IL-6, thus exerting an anti-radiation effect. P53/TLR2 modulator-1 shows significant anti-radiation activity against both AHH-1 cells and HUVECs. It can also increase the survival rate of C57BL/6J mice irradiated with a lethal dose of radiation and reduce the damage to their hematopoietic system, the villous structure of the small intestine, and the spleen caused by radiation. P53/TLR2 modulator-1 can be used in the research of radiation injury-related diseases .
Cat. No.: HY-181413
CAS No.: 3093642-25-9
Research Areas:
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.: HY-B0819
CAS No.: 14816-18-3
Target:
Insecticide Cholinesterase (ChE) Cytochrome P450 Autophagy Reactive Oxygen Species (ROS) Apoptosis Bcl-2 Family Caspase COX Keap1-Nrf2 TNF Receptor Interleukin Related Bacterial
Research Areas:
Phoxim is an organophosphorus pesticide and an orally active inhibitor of cholinesterase and CYP3A, which induces neurotoxicity in Caenorhabditis elegans and causes nephrotoxicity characterized by glomerular atrophy and interstitial fibrosis. Phoxim induces inhibition of the autophagy pathway. Phoxim induces dopaminergic neuron degeneration and exacerbates Aβ-induced paralysis. Phoxim damages enterocytes and disrupts intestinal barrier integrity. Phoxim induces ROS accumulation. Phoxim induces mitochondrial apoptosis, involving upregulation of Bad, Bax, caspase-3, and caspase-9 and downregulation of Bcl-2. Phoxim inhibits mitochondrial functional enzymes (COX, Ca 2+-Mg 2+-ATPase, SDH). Phoxim upregulates Nrf2 mRNA expression in the jejunal mucosa. Phoxim increases TNF-α and decreases IL-6 and IL-8 in the intestinal mucosa. Phoxim alters gut microbial composition by increasing total bacteria and Escherichia coli and reducing Lactobacillus. Phoxim enhances energy metabolism in silver carp by upregulating key glycolytic and gluconeogenic enzymes. Phoxim is used in research on neurodegenerative diseases, nephrotoxicity, intestinal oxidative stress and barrier dysfunction, and bacterial sepsis .
Cat. No.: HY-W075770
CAS No.: 1313-99-1
Synonyms: Nickel monoxide
Target:
Environmental Pollutants Apoptosis Reactive Oxygen Species (ROS) Caspase TGF-beta/Smad p38 MAPK Akt PI3K
Research Areas:
Nickel(II) oxide (nickel monoxide) is a chemical warfare agent that can enter the body through the respiratory tract and other routes, distributing to organs such as the lungs and testes. The nanoparticle form of nickel(II) oxide (NiO NPs) exhibits antibacterial, anti-leishmanial, anti-diabetic, and anti-cancer activities. NiO NPs can be activated by ultraviolet and visible light, generating reactive oxygen species (ROS). Nickel(II) oxide induces oxidative stress by generating reactive oxygen species, activating the TGF-β1-mediated MAPK and PI3K/AKT pathways, disrupting the MMPs/TIMPs balance, and upregulating the expression of inflammatory factors (IL-1β, IL-6) and apoptosis-related molecules (Bax, caspase-3, p53), while inhibiting the activity of the anti-apoptotic molecule Bcl-2. Nickel(II) oxide induces cytotoxicity, promotes fibrosis, triggers inflammatory responses, and causes apoptosis. Nickel(II) oxide can be applied in research on the safety assessment of nanomaterials, such as in the context of pulmonary fibrosis and reproductive system toxicity .
Cat. No.: HY-10032A
CAS No.: 1247874-19-6
Target:
PF-477736 (hydrochloride) is an ATP-competitive Chk1 inhibitor (Ki 0.49 nM) that also inhibits CK2A1, PKCA, and Akt1, and is a broad-spectrum kinase inhibitor .PF-477736 induces apoptosis via PARP cleavage, caspase-3/7 activation, caspase-independent death, BAX and PUMA upregulation, H2AX phosphorylation, DNA fragmentation, and Chk1 proteasomal degradation, while inhibiting proliferation and preventing mitotic entry .PF-477736 demonstrates selective synthetic lethality in LIMD1-deficient cells, efficacy in subcutaneous xenograft models of LIMD1-deficient tumors, and anti-proliferative activity against leukemia and lymphoma cell lines .PF-477736 induces DNA double-strand breaks and activates the ATM-p53-p21 axis, and sensitizes CHK1i-insensitive neuroblastoma cells to apoptosis with ATM or DNA-PK inhibitors .PF-477736 can be used for the research of non-small cell lung cancer, leukemia, lymphoma, and neuroblastoma .
Cat. No.: HY-184378
CAS No.: 2922221-22-3
Target:
Research Areas:
MDB5 is a Hedgehog pathway and Smoothened inhibitor that binds to the 7-TM domain of Smo . MDB5 reduces hepatic stellate cell activation, extracellular matrix-related gene expression, collagen deposition, hydroxyproline content and epithelial-mesenchymal transition, and prevents sinusoidal endothelial cell capillarization . MDB5 induces G1 and S phase cell cycle arrest, triggers apoptosis by upregulating Bax and downregulating Bcl-2, and also decreases oxygen consumption rate, glucose uptake, transglutaminase activity and fibronectin matrix assembly . MDB5 reduces the levels of liver injury markers, hepatic triglyceride deposition and hepatic steatosis, restores the tissue structure of the kidney and spleen, and inhibits pancreatic tumor growth without causing body weight loss . MDB5 can be loaded into PEG-PCC-g-DC micelles, achieving high drug loading, sustained release, improved water solubility, enhanced cellular uptake and optimized hepatic distribution, with good tolerance in mice . MDB5 is applicable to research related to alcohol-associated liver disease, liver fibrosis and pancreatic cancer .
Cat. No.: HY-N0566
CAS No.: 85999-40-2
Synonyms: Anemosapogenin
Cat. No.: HY-P11935
CAS No.: 2410535-57-6
Target:
Wnt Apoptosis Pyroptosis NOD-like Receptor (NLR) Caspase Bcl-2 Family β-catenin GSK-3 Interleukin Related
Research Areas:
RR-171 is an amino acid polypeptide and an inhibitor of the Wnt signaling pathway. RR-171 reduces the expression levels of Wnt-1, GSK3β and β-catenin. RR-171 induces apoptosis (Apoptosis) in pancreatic cancer cells, which is characterized by an increased Bax/Bcl-2 ratio, activation of Caspase-3/7/9, and increased Cleaved-PARP; this pro-apoptotic effect can be partially reversed by Z-VAD-FMK (HY-16658B). RR-171 also induces pyroptosis (Pyroptosis) in pancreatic cancer cells, which is manifested by activation of the NLRP-3 inflammasome, activation of Caspase-1, cleavage of GSDMD, upregulation of IL-1β and IL-18, and increased LDH release; this pro-pyroptotic effect can be partially reversed by VX-765 (HY-13205). RR-171 inhibits the viability, proliferation and colony formation of pancreatic cancer cells, with low cytotoxicity against normal cells. RR-171 downregulates the expression of Ki-67 and PCNA in tumor tissues in vivo, with favorable biosafety. RR-171 can be used in studies related to pancreatic cancer .
Cat. No.: HY-W028393R
CAS No.: 392-12-1
Category:
Cat. No.: HY-176421
CAS No.: 3070438-85-3
Target:
PROTACs PI3K Apoptosis Akt Bcl-2 Family Caspase P-glycoprotein
Research Areas:
PROTAC PI3K/110β degrader-1 is a VHL-recruiting PROTAC degrader targeting PI3K/110β, with DC50 values of 0.416 μM (MCF-7) and 19.66 μM (A549), respectively. PROTAC PI3K/110β degrader-1 recruits VHL to induce proteasomal degradation of PI3K/110β. It activates endoplasmic reticulum stress (ERS)-mediated mitochondrial apoptosis via the PERK/ATF4/CHOP unfolded protein response (UPR) pathway, downregulates p-AKT and Bcl-2, upregulates Bax, cleaved-caspase-9 and cleaved-caspase-3, inhibits the expression and activity of P-gp, and exerts synergistic anti-tumor effects with Doxorubicin (Adriamycin, ADM) (HY-15142A) and Cisplatin (DDP) (HY-17394). PROTAC PI3K/110β degrader-1 can be used in research related to multidrug-resistant cancers .
Cat. No.: HY-182360
Target:
PERK Eukaryotic Initiation Factor (eIF) Bcl-2 Family Apoptosis Reactive Oxygen Species (ROS) STING DNA/RNA Synthesis PD-1/PD-L1
Research Areas:
Cytisine-Platinum(IV) Prodrug-1 is a Pt(IV) prodrug incorporating the natural compound Cytisine (HY-N0175) with antiproliferative activity against tumor cells. Cytisine-Platinum(IV) Prodrug-1 promotes calcium transfer across the IP3R1-GRP75-VDAC1 axis to drive mitochondrial calcium overload. Cytisine-Platinum(IV) Prodrug-1 initiates unfolded protein response via PERK, eIF2α, ATF4, and CHOP to modulate Bcl-2 and Bax, triggering apoptosis. Cytisine-Platinum(IV) Prodrug-1 induces mitochondrial dysfunction, ROS production, reduced ATP synthesis, DNA damage, and S-phase cell cycle arrest. Cytisine-Platinum(IV) Prodrug-1 activates the cGAS-STING pathway, reduces PD-L1 expression, drives immunogenic cell death. Cytisine-Platinum(IV) Prodrug-1 exhibits high physiological stability, efficient cellular accumulation, and enhanced platinum-DNA binding, and inhibits tumor growth in mouse models with reduced systemic toxicity. Cytisine-Platinum(IV) Prodrug-1 can be used for the research of lung cancer .
Cat. No.: HY-N0566R
CAS No.: 85999-40-2
Synonyms: Anemosapogenin (Standard)
Category:
Cat. No.: HY-W758414
Phoxim-d5 (phenyl-d5) (mixture of isomers) is the deuterated-labeled Phoxim (HY-B0819). Phoxim is an organophosphorus pesticide and an orally active inhibitor of cholinesterase and CYP3A, which induces neurotoxicity in Caenorhabditis elegans and causes nephrotoxicity characterized by glomerular atrophy and interstitial fibrosis. Phoxim induces inhibition of the autophagy pathway. Phoxim induces dopaminergic neuron degeneration and exacerbates Aβ-induced paralysis. Phoxim damages enterocytes and disrupts intestinal barrier integrity. Phoxim induces ROS accumulation. Phoxim induces mitochondrial apoptosis, involving upregulation of Bad, Bax, caspase-3, and caspase-9 and downregulation of Bcl-2. Phoxim inhibits mitochondrial functional enzymes (COX, Ca 2+-Mg 2+-ATPase, SDH). Phoxim upregulates Nrf2 mRNA expression in the jejunal mucosa. Phoxim increases TNF-α and decreases IL-6 and IL-8 in the intestinal mucosa. Phoxim alters gut microbial composition by increasing total bacteria and Escherichia coli and reducing Lactobacillus. Phoxim enhances energy metabolism in silver carp by upregulating key glycolytic and gluconeogenic enzymes. Phoxim is used in research on neurodegenerative diseases, nephrotoxicity, intestinal oxidative stress and barrier dysfunction, and bacterial sepsis .
Cat. No.: HY-184501
CAS No.: 486440-74-8
UE01 is an orally active, selective small-molecule modulator targeting both ULK1/ERK1/2. UE01 activates hULK1 with an EC50 of 695.30 nM and a KD of 114.3 nM for ULK1; it inhibits hERK1 with an IC50 of 179.90 nM and a KD of 114 nM for ERK1; it shows weak binding to ERK2 with a KD of 2.8 mM. UE01 induces the conformational transition of ULK1 from an inactive to an active state, enhances the phosphorylation of ULK1 Ser317 and mAtg13 Ser355, and reduces the phosphorylation of ULK1 Ser757. UE01 competitively occupies the ATP-binding pocket of ERK1, inhibits ERK1 kinase activity, and reduces the activity of the ERK1/2 signaling pathway. UE01 induces complete autophagy flux and apoptosis, upregulates Atg5, Atg7, LC3-II/LC3-I, Bax, cytochrome C (Cyt c), Cleaved-Caspase 3, Cleaved-PARP1 and E-cadherin, downregulates p62, Bcl-2, MMP-2 and MMP-9, reduces the phosphorylation of Exo70 Ser250, and promotes the proteasome-dependent degradation of Cav-1, thereby inhibiting EMT-related phenotypes and extracellular matrix degradation. UE01 can be used in studies related to triple-negative breast cancer .
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Protocols
Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!A suitable model is crucial in drug screening experiments. Organs can mimic the three-dimensional functional structure of internal organs, have similar spatial organization to corresponding organs, maintain some key characteristics, and reproduce some physiological functions. They are widely used for modeling and personalized drug screening physiological functions.2025-02-06
