myc-in-2

MYC-IN-2 is a protein-protein inhibitor targeting the MYC protein, designed for use in cancer research.

WDR5-MYC-IN-2 is an inhibitor of the WDR5-MYC protein-protein interaction (PPI) with an IC50 of 0.59 μM. It is utilized in research on MYC-driven cancers and in the development of other potent WDR5-MYC PPI inhibitors.

Puromycin dihydrochloride (CL13900 dihydrochloride) is a cinnamamide adenosine antibiotic and an inhibitor of protein synthesis. Puromycin dihydrochloride inhibits protein synthesis by binding to RNA and has antitumor and antitrypanosomal activity.

6-fluorinated inated-aristeromycin2c showed antiviral activity against heat virus, Zika virus and Sars coronavirus.

Spectinomycin dihydrochloride (Actinospectacin) is an antibiotic produced by Streptomyces spectabilis. It is active against gram-negative bacteria and used for the treatment of gonorrhea.

Clindamycin Phosphate is the phosphate salt form of clindamycin, a semi-synthetic, chlorinated broad-spectrum antibiotic produced by chemical modification of lincomycin. Clindamycin phosphate (Clindamycin 2-dihydrogen phosphate) is used in topical preparations.

Erythromycin 2'-propionate is a macrolide antibiotic and an esterified form of erythromycin .1It is active againstS. aureuswhen used at a concentration of 1 μg/ml. Erythromycin 2'-propionate (1 mM) inhibits protein synthesis in a cell-free assay. 1.Tardrew, P.L., Mao, J.C.H., and Kenney, D.Antibacterial activity of 2'-esters of erythromycinAppl. Microbiol.18(2)159-165(1969)

Clindamycin phosphate (Standard) is the standard substance of Clindamycin phosphate, and it is applicable for quantitative analysis, quality control, and related research in biochemical experiments. Clindamycin Phosphate is the phosphate salt form of clindamycin, a semi-synthetic, chlorinated broad-spectrum antibiotic produced by chemical modification of lincomycin. Clindamycin phosphate (Clindamycin 2-dihydrogen phosphate) is used in topical preparations.

Pacidamycin 2 exhibits inhibitory effects against Pseudomonas aeruginosa. It also affects a limited number of other bacterial strains, including Staphylococcus aureus and Escherichia coli.

Clindamycin 2,4-diphosphate is a reagent used in biochemical reactions.

CBP/EP300-IN-2 is an inhibitor of CBP/EP300 with IC50 values of 1.07 nM for CBP/HTRF and 5.96 nM for Myc.

LZZ-02 inhibits the transcriptional activity of β-catenin by stabilizing axin 2 and reducing the levels of downstream proteins, including c-Myc and cyclin D1, which leads to the degradation of β-catenin. This results in the effective reduction of tumor xenografts derived from colon cell lines.

FTO-IN-13 (compound 8t) is a potent FTO inhibitor with antiproliferative properties. It induces apoptosis (cell apoptosis) and reduces the expression of Bcl-2 and Caspase 3 active proteins. Additionally, FTO-IN-13 lowers the expression of MYC and CEBPA genes and demonstrates anticancer activity.

HDAC3/BRD4-IN-1 (compound 26n) is an inhibitor of HDAC3/BRD4, exhibiting an IC50 of 8 nM for HDAC3, while its IC50 values for HDAC1 and HDAC2 are 220 nM and 120 nM, respectively. It displays anti-tumor and anti-proliferative effects by upregulating Ac-H3 and downregulating c-Myc. The half-life of HDAC3/BRD4-IN-1 in human liver microsomes is 29.36 minutes.

ERK1/2 inhibitor 10 (Compound 36c) is a potent inhibitor of ERK1 and ERK2, with IC50 values of 0.11 nM and 0.08 nM, respectively. It effectively hinders the phosphorylation of downstream substrates p90RSK and c-Myc. Additionally, ERK1/2 inhibitor 10 induces apoptosis and incomplete autophagy-related cell death. This compound demonstrates significant antitumor efficacy in models of triple-negative breast cancer and colorectal cancer harboring BRAF and RAS mutations.

FKBP12 ligand-2 (compound d) is a high-affinity ligand that targets FKBP12. This compound is utilized to selectively enhance the binding of heterobifunctional molecules to BRD4, facilitating the intracellular accumulation of drugs through the "CellTrap" effect. It forms a ternary complex of FKBP12-ligand-BRD4, which inhibits BRD4, suppresses the expression of BRD4 target genes such as MYC, and induces tumor cell death. FKBP12 ligand-2 is applicable in selective cancer research based on the differential levels of presenter proteins within cells.

c-MYC/BCL2 ligand 1 iodide is a dual-target ligand that specifically interacts with the G-quadruplex (G4) regions of the c-MYC and Bcl-2 promoters, exhibiting Kd values of 0.90 μM for c-MYCG4 and 0.56 μM for Bcl-2G4. It works by binding to these G4-forming sequences to inhibit transcription of the c-MYC and Bcl-2 genes, leading to reduced protein expression. This compound effectively suppresses MCF-7 cell proliferation and migration, induces G1 phase cell cycle arrest, and triggers apoptosis. Additionally, it significantly hampers tumor growth in the 4T1 homogenous model with negligible toxicity. c-MYC/BCL2 ligand 1 iodide is applicable in breast cancer research.

I3IN-002 is a small molecule inhibitor targeting the RNA-binding protein IGF2BP3, with an IC50 value of approximately 2 μM in SEM cells. It disrupts the interaction with m6A-modified mRNA, destabilizing target genes (such as CDK6, MYC, and BCL2), thereby inhibiting the growth of leukemia cells, inducing cell cycle arrest, and promoting apoptosis. I3IN-002 shows potential for research in B-cell acute lymphoblastic leukemia.

PROTAC BRD4 Degrader-8 is a potent BRD4 inhibitor with IC50 values of 1.1 nM and 1.4 nM for BRD4 BD1 and BD2, respectively, effectively degrading the BRD4 protein in PC3 prostate cancer cells[1].

Nemorosone is a polycyclic polyprenylated acylphloroglucinol (PPAP) originally isolated from C. rosea that has antiproliferative properties.1 Nemorosone inhibits growth of NB69, Kelly, SK-N-AS, and LAN-1 neuroblastoma cells (IC50s = 3.1-6.3 μM), including several drug-resistant clones, but not MRC-5 human embryonic fibroblasts (IC50 = >40 μM).2 It increases DNA fragmentation in LAN-1 cells in a dose-dependent manner, and decreases N-Myc protein levels and phosphorylation of ERK1/2 by MEK1/2. Nemorosone also inhibits growth of Capan-1, AsPC-1, and MIA-PaCa-2 pancreatic cancer cells (IC50s = 4.5-5.0 μM following a 72-hour treatment) but not human dermal and foreskin fibroblasts (IC50s = >35 μM).1 It induces apoptosis, abolishes the mitochondrial membrane potential, and increases cytosolic calcium concentration in pancreatic cancer cells in a dose-dependent manner. Nemorosone activates the caspase cascade in a dose-dependent manner and inhibits cell cycle progression, increasing the proportion of cells in the G0/G1 phase, in both neuroblastoma and pancreatic cancer cells.1,2 Nemorosone (50 mg/kg, i.p., per day) also reduces tumor growth in an MIA-PaCa-2 mouse xenograft model.3References1. Holtrup, F., Bauer, A., Fellenberg, K., et al. Microarray analysis of nemorosone-induced cytotoxic effects on pancreatic cancer cells reveals activation of the unfolded protein response (UPR). Br. J. Pharmacol. 162(5), 1045-1059 (2011).2. Díaz-Carballo, D., Malak, S., Bardenheuer, W., et al. Cytotoxic activity of nemorosone in neuroblastoma cells. J. Cell. Mol. Med. 12(6B), 2598-2608 (2008).3. Wold, R.J., Hilger, R.A., Hoheisel, J.D., et al. In vivo activity and pharmacokinetics of nemorosone on pancreatic cancer xenografts. PLoS One 8(9), e74555 (2013). Nemorosone is a polycyclic polyprenylated acylphloroglucinol (PPAP) originally isolated from C. rosea that has antiproliferative properties.1 Nemorosone inhibits growth of NB69, Kelly, SK-N-AS, and LAN-1 neuroblastoma cells (IC50s = 3.1-6.3 μM), including several drug-resistant clones, but not MRC-5 human embryonic fibroblasts (IC50 = >40 μM).2 It increases DNA fragmentation in LAN-1 cells in a dose-dependent manner, and decreases N-Myc protein levels and phosphorylation of ERK1/2 by MEK1/2. Nemorosone also inhibits growth of Capan-1, AsPC-1, and MIA-PaCa-2 pancreatic cancer cells (IC50s = 4.5-5.0 μM following a 72-hour treatment) but not human dermal and foreskin fibroblasts (IC50s = >35 μM).1 It induces apoptosis, abolishes the mitochondrial membrane potential, and increases cytosolic calcium concentration in pancreatic cancer cells in a dose-dependent manner. Nemorosone activates the caspase cascade in a dose-dependent manner and inhibits cell cycle progression, increasing the proportion of cells in the G0/G1 phase, in both neuroblastoma and pancreatic cancer cells.1,2 Nemorosone (50 mg/kg, i.p., per day) also reduces tumor growth in an MIA-PaCa-2 mouse xenograft model.3 References1. Holtrup, F., Bauer, A., Fellenberg, K., et al. Microarray analysis of nemorosone-induced cytotoxic effects on pancreatic cancer cells reveals activation of the unfolded protein response (UPR). Br. J. Pharmacol. 162(5), 1045-1059 (2011).2. Díaz-Carballo, D., Malak, S., Bardenheuer, W., et al. Cytotoxic activity of nemorosone in neuroblastoma cells. J. Cell. Mol. Med. 12(6B), 2598-2608 (2008).3. Wold, R.J., Hilger, R.A., Hoheisel, J.D., et al. In vivo activity and pharmacokinetics of nemorosone on pancreatic cancer xenografts. PLoS One 8(9), e74555 (2013).

Idarubicin, a potent anthracycline antileukemic agent, is orally active in its application. It functions by inhibiting topoisomerase II, thus interfering with DNA replication and RNA transcription. Furthermore, Idarubicin induces DNA damage, inhibits DNA synthesis, and suppresses c-myc expression. It also demonstrates inhibitory effects on the growth of bacteria and yeasts [1] [2] [3] [4] [5].

BRD4 Inhibitor-15 (compound 13) is a highly potent and specific BRD4 inhibitor with an IC50 of 18 nM, inducing apoptosis in 22RV1 cells by regulating Bcl-2/Bax proteins and activating caspase-3 signaling, and down-regulating c-Myc levels, making it valuable for prostate cancer research [1].

P300 bromodomain-IN-1 is a potent inhibitor of p300 (EP300) bromodomain (IC50: 49 nM). p300 bromodomain-IN-1 blocks c-Myc expression and induces cell cycle arrest at G1/G0 phase and apoptosis in OPM-2 cells. apoptosis).

MRK003 is a γ-secretase inhibitor exhibits promising in vitro pre-clinical activity in multiple myeloma and non-Hodgkin's lymphoma. MRK003 treatment induced caspase-dependent apoptosis and inhibited proliferation of MM and NHL cell lines and patient cells. Examination of signaling events after treatment showed time-dependent decrease in levels of the notch intracellular domain, Hes1 and c-Myc. MRK003 downregulated cyclin D1, Bcl-Xl and Xiap levels in NHL cells and p21, Bcl-2 and Bcl-Xl in MM cells. In addition, MRK003 caused an upregulation of pAkt, indicating crosstalk with the PI3K/Akt pathway.