Acute Myeloid Leukemia

Decitabine (NSC 127716) is an orally active deoxycytidine analogue antimetabolite and DNA methyltransferase inhibitor. Decitabine incorporates into DNA in place of cytosine can covalently trap DNA methyltransferase to DNA causing irreversible inhibition of the enzyme. Decitabine induces cell G2/M arrest and cell Apoptosis. Decitabine has potent anticancer activity.

Tocilizumab (Anti-Human IL6R, Humanized Antibody) is an anti-human interleukin-6 receptor (IL-6R) neutralizing antibody, prevents binding of IL-6 to the IL-6R, thereby inhibiting both classic and trans-signaling. Tocilizumab (Anti-Human IL6R, Humanized Antibody) can be used for the treatment of rheumatoid arthritis. Tocilizumab is remarkablely effective for the study of severe COVID-19 (coronavirus disease).

Busulfan is a potent alkylating antineoplastic agent. Busulfan causes DNA damage by cross-linking DNAs and DNA and proteins. Busulfan inhibits thioredoxin reductase. Busulfan induces apoptosis. Busulfan is an immunosuppressive and myeloablative chemotherapeutic agent.

GCN2iB is an ATP-competitive, selective GCN2 inhibitor with an IC₅₀ of 2.4 nM. GCN2iB inhibits the activation of the GCN2 pathway and upregulates GPX4. GCN2iB enhances the anticancer effect of ASNase against acute lymphoblastic leukemia. GCN2iB increases left ventricular ejection fraction, while reducing fasting blood glucose and myocardial fibrosis. GCN2iB can be used in research related to acute lymphoblastic leukemia, acute myeloid leukemia and diabetic cardiomyopathy.

Idasanutlin (RG7388) is an orally bioavailable MDM2 inhibitor with an IC₅₀ of 6 nM. Idasanutlin disrupts MDM2-p53 binding, stabilizes and activates p53, triggering cell cycle arrest, apoptosis, and reduced cancer cell viability. Idasanutlin reduces EGFR protein expression and phosphorylation, suppresses downstream SHP2, MEK1/2, ERK1/2, AKT, mTOR, p70(S6K1), and S6 signaling. Idasanutlin induces mitochondrial ROS production, drives p38 MAPK phosphorylation, upregulates NOXA, and mediates caspase-3-dependent apoptosis and gasdermin E-mediated pyroptosis. Idasanutlin can be used for the research of TP53-mutant non-small cell lung cancer, T-cell acute lymphoblastic leukemia, colorectal carcinoma, melanoma, diffuse large B-cell lymphoma, mantle cell lymphoma, non-Hodgkin lymphoma, severe fever with thrombocytopenia syndrome, neuroblastoma, acute lymphoblastic leukemia, relapsed or refractory acute myeloid leukemia, osteosarcoma, solid tumors, and hematological tumors.

FPFT-2216 is an orally active Molecular glue degrader targeting IKZF1, IKZF3, CK-1α, and PDE6D, with a DC₅₀ of 8 nM against PDE6D. FPFT-2216 mediates ubiquitin-proteasome degradation via the CRL4^CRBN E3 ubiquitin ligase complex and interacts with the non-isoprenoid-binding region of PDE6D. FPFT-2216 activates the p53 signaling pathway, inhibits the CBM complex/NF-κB pathway, upregulates IL-2, suppresses IL-1β and IL-6, and induces tumor cell Apoptosis. FPFT-2216 exhibits anticancer activity against multiple myeloma and lymphoma. FPFT-2216 can be used in research related to multiple myeloma, lymphoma, acute lymphoblastic leukemia, acute myeloid leukemia, pancreatic ductal adenocarcinoma, non-small cell lung cancer, and gastric adenocarcinoma.

Cyproheptadine acts as a p38 MAP kinase activator, CHK2 activator, histamine H1 receptor inhibitor and serotonin receptor inhibitor. Cyproheptadine mediates cell cycle arrest via G1 phase arrest, G1/S transition arrest, G0/G1 phase arrest, reduced expression of cyclins D1/D2/D3, upregulated expression of HBP1, p16, p21, p27, and decreased phosphorylation of retinoblastoma protein. Cyproheptadine induces Apoptosis by increasing PARP and cleaved PARP, as well as activating the mitochondrial caspase pathway. Cyproheptadine inhibits tumor growth with extremely low toxicity to normal cells. Cyproheptadine can be used in research related to hepatocellular carcinoma, multiple myeloma and acute myeloid leukemia.

Cyproheptadine hydrochloride (Cyproheptadine HCl) acts as a p38 MAP kinase activator, CHK2 activator, histamine H1 receptor inhibitor and serotonin receptor inhibitor. Cyproheptadine hydrochloride mediates cell cycle arrest via G1 phase arrest, G1/S transition arrest, G0/G1 phase arrest, reduced expression of cyclins D1/D2/D3, upregulated expression of HBP1, p16, p21, p27, and decreased phosphorylation of retinoblastoma protein. Cyproheptadine hydrochloride induces Apoptosis by increasing PARP and cleaved PARP, as well as activating the mitochondrial caspase pathway. Cyproheptadine hydrochloride inhibits tumor growth with extremely low toxicity to normal cells. Cyproheptadine hydrochloride can be used in research related to hepatocellular carcinoma, multiple myeloma and acute myeloid leukemia.

FHD-286 is a selective, oral inhibitor of SMARCA4/SMARCA2 ATPase (BRG1 and BRM) inhibitor. FHD-286 has the potential for the research of BAF (BRG1/BRM-associated factor)-related disorders such as acute myeloid leukemia.

Rituximab (anti-CD20) is an anti-CD20 chimeric monoclonal antibody used to treat certain autoimmune diseases and types of cancer.

Gemtuzumab ozogamicin is an antibody-drug conjugate (ADC) consisting of a humanized immunoglobulin (IgG4) antibody directed against CD33 that is conjugated to the cytotoxic agent Calicheamicin (HY-19609). The antibody portion is Gemtuzumab (HY-P99971), and the drug-linker conjugate for ADC is N-Ac-γ-Calicheamicin-AcBut-NHS ester (HY-103688). Gemtuzumab ozogamicin can be used for the research of acute myeloid leukemia (AML).

FHD-609 is a BRD9 PROTAC degrader. FHD-609 induces BRD9 degradation, downregulates primary transcripts of HBG/HBD, Myc expression and proliferation gene sets, reduces the levels of synovial sarcoma tumor proliferation markers, and inhibits tumor growth. FHD-609 can be used in research related to advanced synovial sarcoma, SMARCB1-deficient tumors and adrenocortical carcinoma.

Mivebresib (ABBV-075) is a potent and orally active bromodomain and extraterminal domain (BET) bromodomain inhibitor. Mivebresib binds to BRD4 with a K_i of 1.5 nM.

MS177 is an effective and fast-acting EZH2 degrader. MS177 is a PROTAC that consists of a CRBN ligand, linker, and a potent enzymatic EZH2 inhibitor C24 (C24 IC₅₀): 12 nM). MS177 effectively depletes both canonical EZH2-PRC2 and noncanonical EZH2-cMyc complexes. MS177 induces leukaemia cell growth inhibition, apoptosis and cell cycle progression arrest.

Dihomo-γ-linolenic acid (DGLA) is a 20-carbon ω-6 fatty acid, with anti-inflammatory and anti-proliferative activities. Dihomo-γ-linolenic acid attenuates atherosclerosis in the apolipoprotein E deficient mouse model system.

AK-2292 is a potent and selective STAT5 PROTAC degrader, with a DC₅₀ of 0.10 μM. AK-2292 induces degradation of STAT5A/B proteins in vitro and in vivo. AK-2292 can induce tumor regression in acute myeloid leukemia and chronic myeloid leukemia xenograft mouse models. AK-2292 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.

Siremadlin (NVP-HDM201) is a potent, orally bioavailable and highly specific p53-MDM2 interaction inhibitor.

Basiliximab (CHI 621) is a recombinant chimeric murine/human IgG1 monoclonal anti-interleukin-2 receptor antibody. Basiliximab can be used for the research of renal transplantation.

CFT8634 is an orally active BRD9 PROTAC degrader with a DC₅₀ of 0.003 μM (HEK293T.166). CFT8634 recruits the CRBN E3 ubiquitin ligase to form a ternary complex, triggering CRBN-catalyzed BRD9 polyubiquitination and 26S proteasome-mediated degradation. CFT8634 induces sustained tumor regression and inhibits tumor growth in mouse models. CFT8634 can be used in research related to synovial sarcoma, SMARCB-1-deficient cancers, acute myeloid leukemia, malignant rhabdoid tumors, and multiple myeloma.

Cusatuzumab (ARGX-110) is a selective competitive blocker targeting CD70 (with an equilibrium dissociation constant of 17 pM for binding to human CD70). Cusatuzumab also possesses enhanced antibody-dependent cell-mediated cytotoxicity (ADCC) activity. It is a humanized IgG1 monoclonal antibody, artificially synthesized through humanization and genetic engineering modifications (CH2 region mutation to enhance effector function). Cusatuzumab has a dual mechanism of action: firstly, it competitively blocks the interaction between CD70 and CD27, inhibiting the CD27-NF-κB signaling pathway, reducing regulatory T cell (Treg) activation and tumor cell proliferation; secondly, by enhancing binding to FcγRIIIa, it mediates ADCC and antibody-dependent cellular phagocytosis (ADCP), directly lysing CD70-positive tumor cells. Cusatuzumab can efficiently eliminate leukemia stem cells (LSCs), induce tumor cell differentiation and apoptosis, restore immune surveillance, and target CD70-positive tumors. Cusatuzumab is used in the study of acute myeloid leukemia (AML).