MDM-2/p53 Activator

CPT2 (Carnitine palmitoyltransferase 2), an enzyme that participates in fatty acid oxidation, also is a colorectal cancer (CRC) prognostic biomarker. CPT2 overexpression can activate p-p53 to increase p53 expression, thereby inhibiting tumor proliferation and promoting apoptosis. CPT2 deficiency results in the most common inherited disorder of long-chain fatty acid oxidation affecting skeletal muscle. Downregulation of CPT2 is also highly correlated with the progression of various cancers and has potential for cancer research.

MB725 is an ethylamide analogue of MB710 (HY-120373). MB725 increases mRNA levels of a range of p53 target genes, notably PUMA, p21, MDM2, NOXA and BAX. MB725 shows selective anticancer activity against p53-Y220C cancer.

JR4-187 is an orally active, copper-dependent anticancer agent. JR4-187 downregulates genes involved in oxidative phosphorylation, MYC targets and E2F targets in cancer cells, while upregulates genes involved in the TNF-α signaling pathway, p53 pathway and KRAS signaling pathway, and downregulates CTR1 protein. JR4-187 induces ROS production, apoptosis, copper-dependent cytotoxicity, and exhibits selective cytotoxicity against KRAS-mutant cancer cells. JR4-187 is well tolerated in mouse models of pancreatic cancer. JR4-187 can be used in research related to cancers such as pancreatic ductal adenocarcinoma, colon cancer and rectal cancer.

p53 Activator 17 is a p53-Y220C activator. p53 Activator 17 exhibits selective cytotoxicity and pro-apoptotic activity in p53-Y220C mutant cancer cell lines, with minimal effects in wild-type or p53-null cells. p53 Activator 17 induces a mutant-to-wild-type conformational shift in cellular p53-Y220C, accompanied by transcriptional activation of canonical p53 target genes, including BBC3 (PUMA) and MDM2. p53 Activator 17 can be used for the study of hepatocellular carcinoma and breast cancer.

CX-5461 hydrochloride is a selective, orally active RNA polymerase I inhibitor. CX-5461 hydrochloride disrupts the formation of the SL1-rDNA complex, thereby blocking the transcription initiation of ribosomal RNA without altering the activity of RNA polymerase II, DNA replication, or protein translation processes. CX-5461 hydrochloride upregulates the expression of p21, MDM2, Sestrin1/2, and phosphorylated AMPKα, and reduces the level of phosphorylated Akt. CX-5461 hydrochloride induces G2/G2/M cell cycle arrest, Autophagy, Apoptosis, and cellular senescence, and activates CHK1, CHK2, and RPA. CX-5461 hydrochloride can be used in research related to osteosarcoma, cervical cancer, hematologic malignancies, high-grade serous ovarian cancer, and solid tumors.

Higenamine-d₄-1 (Norcoclaurine-d₄-1) hydrochloride is deuterium labeled Higenamine (hydrochloride). Higenamine hydrochloride is a selective LSD1 inhibitor (IC₅₀=1.47 μM) that can be isolated from aconite. Higenamine hydrochloride has anti-inflammatory and antibacterial activity. Higenamine (Norcoclaurine) can attenuate IL-1β-induced Apoptosis through ROS-mediated PI3K/Akt signaling pathway. Higenamine hydrochloride protects brain cells from oxygen deprivation. Higenamine can promote bone formation in osteoporosis through the SMAD2/3 pathway. Higenamine hydrochloride can be used to study cancer, inflammation, cardiorenal syndrome and other diseases.

S-Diclofenac (Standard) is the analytical standard of S-Diclofenac. This product is intended for research and analytical applications. S-Diclofenac (ACS 15) is a hybrid molecule of an H2S donor and the NSAID diclofenac. S-Diclofenac activates the p53 signaling pathway, and inhibits the activation of JNK. S-Diclofenac exhibits antioxidant and anti-inflammatory activities.

Americanin A is a Neolignan. Americanin A can be isolated from the seeds of Phytolacca americana. Americanin A activates ATM and ATR, initiating the subsequent signal transduction cascades that include Chk1, Chk2, and tumor suppressor p53. Americanin A targets selectively Skp2 for degradation and thereby stabilizes p27. Americanin A suppresses the activity of Cyclin B1 and its partner cdc2 to prevent entry into Mitosis. Americanin A induces Apoptosis by producing excessive ROS. Americanin A has anti-cancer activity against colorectal cancer.

CGC-11144 hydrochloride is a polyamine analog. CGC-11144 hydrochloride reduces the kinase activities of CDK4, CDK2 and CDK6, induces activation of the p53 pathway and p53-dependent p21 expression, and mediates cell cycle regulation, growth inhibition and apoptosis. CGC-11144 hydrochloride induces G1 phase cell cycle arrest, downregulates cyclin D1 and cyclin B1, upregulates cyclin E, induces dephosphorylation of pRb, and inhibits ERα-mediated transcriptional activity by disrupting the DNA binding of Sp1/Sp3 to the ERα promoter, while also stimulating activation of the JNK/AP-1 pathway. CGC-11144 hydrochloride can be used in research related to breast cancer, choroidal neovascularization and cancer.

Chlorphoxim is a broad-spectrum and highly efficient insecticide. Chlorphoxim kills pests by inhibiting AChE. Chlorphoxim inhibits the activities of SOD and CAT in zebrafish embryos. Chlorphoxim induces oxidative stress in zebrafish embryos by activating ROS. Chlorphoxim induces apoptosis by upregulating the expression levels of Bax, Bcl2 and p53 in zebrafish embryos. Chlorphoxim exhibits neurotoxicity and developmental toxicity. Chlorphoxim is used in agricultural research for the control of various pests.

YW3-56 (hydrochloride) is a PAD inhibitor. YW3-56 (hydrochloride) activates p53 target genes. YW3-56 (hydrochloride) activates ATF and blocks autophagy flux. YW3-56 induces ER stress through the PERK-eIF2α-ATF4 signaling cascade and inhibits the mTOR signaling. YW3-56 (hydrochloride) inhibits triple-negative breast cancer.

Polyporenic acid C (Standard) is an analytical standard of Polyporenic acid C (HY-N2993). This product is intended for research and analytical applications. Polyporenic acid C is a lanostane-type triterpenoid. Polyporenic acid C can be isolated from Poria cocos. Polyporenic acid C causes the cleavage of caspase-8 and caspase-3, as well as the cleavage of PARP. Polyporenic acid C reduces the phosphorylation level of Akt (Ser473), increases the phosphorylation of PTEN and p53 (Ser15), and activates JNK. Polyporenic acid C induces Apoptosis. Polyporenic acid C shows anticancer activity against non-small cell lung cancer.

Higenamine (hydrochloride) (Standard) is the analytical standard of Higenamine (hydrochloride). This product is intended for research and analytical applications. Higenamine hydrochloride is a selective LSD1 inhibitor (IC50=1.47 μM) that can be isolated from aconite. Higenamine hydrochloride has anti-inflammatory and antibacterial activity. Higenamine (Norcoclaurine) can attenuate IL-1β-induced Apoptosis through ROS-mediated PI3K/Akt signaling pathway. Higenamine hydrochloride protects brain cells from oxygen deprivation. Higenamine can promote bone formation in osteoporosis through the SMAD2/3 pathway. Higenamine hydrochloride can be used to study cancer, inflammation, cardiorenal syndrome and other diseases.

Bromuconazole is a triazole fungicide with oral efficacy and blood-brain barrier permeability. Bromuconazole protects crops from various fungal contaminations. Bromuconazole exhibits cytotoxicity against a variety of cancer cells, induces G0/G1 cell cycle arrest and inhibits DNA synthesis in cancer cells, and triggers cytoskeletal structural disorder, genotoxic damage, apoptotic (apoptosis) cell death, and mitochondrial membrane depolarization. Bromuconazole activates caspase-3, induces excessive production of ROS, p53 and Bax, lipid peroxidation, increased activities of SOD and CAT, and downregulates Bcl-2. By upregulating p-ERK1/2 and p-JNK, Bromuconazole disrupts the MAPK signaling pathway, impairs the cellular stress response of human trophoblast cells and endometrial cells, and damages the implantation process. Bromuconazole is applicable to research related to glioma, colon cancer, reproductive injury (implantation dysfunction), and cardiac dysfunction.

Higenamine (Norcoclaurine), a β2-AR agonist with antioxidant capability, is a key component of the Chinese herb aconite root that prescribes for treating symptoms of heart failure in the oriental Asian countries. Higenamine is also a α1-adrenergic receptor antagonist with hypotensive effect. is a selective LSD1 inhibitor (IC50=1.47 μM) that can be isolated from aconite. Higenamine hydrochloride has anti-inflammatory and antibacterial activity. Higenamine protects myocyte Apoptosis and ischemia/reperfusion (I/R) injury through selective activation of beta2-adrenergic receptor (β2-AR). Higenamine also reduces I/R-induced myocardial infarction in mice. Higenamine can attenuate IL-1β-induced Apoptosis through ROS-mediated PI3K/Akt signaling pathway. Higenamine protects brain cells from oxygen deprivation. Higenamine can promote bone formation in osteoporosis through the SMAD2/3 pathway. Higenamine can be used to study cancer, inflammation, cardiorenal syndrome and other diseases.

Lenalidomide-d₄ (CC-5013-d₄) is the d₄-labeled Lenalidomide (HY-A0003). Lenalidomide (CC-5013) is an orally active immunomodulatory agent that binds CRBN as a molecular glue to alter substrate specificity, inducing ubiquitination and proteasome-dependent degradation of IKZF1, IKZF3 and CK1α. Lenalidomide induces apoptosis by degrading IKZF1/3, and activates p53 by degrading CK1α. Lenalidomide promotes IL-2 release and effector functions of CD8⁺ T/NK cells, while inhibiting TNF-α secretion and M1-type pyroptosis. Lenalidomide can be used in research related to hematological malignancies, acute liver failure and acute kidney injury.

Pretilachlor (Standard) is the analytical standard of Pretilachlor (HY-B2035). This product is intended for research and analytical applications. Pretilachlor is a chloroacetamide herbicide with biological activities including endocrine disruption, oxidative stress induction, apoptosis induction, and immunotoxicity. Pretilachlor exerts its effects by interfering with hormone metabolism, inducing oxidative stress, activating apoptotic pathways, and inhibiting immune functions. Pretilachlor upregulates the transcription of P53, Mdm2, and Bbc3, and increases the activities of Caspase3 and Caspase9; it upregulates the transcription of genes in the HPG/HPT axis and the activity of aromatase; it induces oxidative stress, elevates ROS levels, and upregulates CAT, SOD, and GPX. Pretilachlor downregulates the transcription of CXCL-C1C, IL-1β, and IL-8. Pretilachlor disrupts the normal physiological processes and embryonic development of fish, exhibiting significant toxicity. Pretilachlor can be used in studies related to weeding, environmental pollution, and behavioral toxicity in fish.

N-Desmethyl clomipramine-d₇ (Desmethylclomipramine-d₇; Norclomipramine-d₇) is the deuterated-labeled N-Desmethyl clomipramine (HY-12388). N-Desmethyl clomipramine is the orally active major active metabolite of the tricyclic antidepressant Clomipramine (HY-B0457A), possessing multiple activities including anti-inflammatory, antioxidant, antibacterial, and antiparasitic effects. N-Desmethyl clomipramine blocks autophagosome-lysosome fusion, leading to the accumulation of LC3-II, p62, ATG7, WIPI2, and ATG5-12, reactivates the p53/p21 pathway, induces apoptosis through C-PARP and C-CAS3, and inhibits the proliferation, migration, and invasion of renal cancer cells. N-Desmethyl clomipramine inhibits LdTOPIA, inducing R-loop accumulation in the nucleus of Leishmania, ultimately causing parasite death. N-Desmethyl clomipramine can be used for research on depression, metastatic renal cell carcinoma, and leishmaniasis.

dsP53-285 saRNA is a small activating RNA (saRNA) that readily activates wild-type p53 expression by targeting its promoter. dsP53-285 saRNA suppresses bladder cancer cells growth and metastasis.

RKS262 is an orally active cyclin/CDK inhibitor. RKS262 is also an apoptosis inducer and cell cycle regulator, exhibiting cytotoxic activity against cancer cells. RKS262 induces caspase-3 cleavage, ROS generation, SAPK/JNK activation, and upregulates the expression of p53, Bid, Bad, Bok, and p27. RKS262 inhibits the expression of Bcl-2, Mcl-1, Bcl-xL, p21, cyclin D1, cyclin B1, cdc-2, cyclin D4, and DNA-pk KU-80 subunit. RKS262 suppresses the phosphorylation of the IGF-1R/PI3K/PKC pathway, ras oncogene activity, and Cdk-6, while increasing total Akt expression. RKS262 induces G₂/M or S phase cell cycle arrest, disrupts mitochondrial transmembrane potential, and reduces tumor burden in xenograft models. RKS262 is used in research on neuroblastoma and ovarian cancer.