mv 1

MV1 is an antagonist of IAP. When combined with HaloTag ligand, MV1 causes protein knockdown of HaloTag-fused proteins.

MV-1-NH-Me, an MV-1-derived IAP ligand, connects to an ABL inhibitor through a linker, resulting in the formation of SNIPER[1].

M-808 is a potent and efficacious covalent inhibitor, targeting the interaction between Menin and MLL. It demonstrates a high binding affinity with an IC50 value of 2.6 nM.

ORY-1001 is a KDM1A inhibitor (IC50 <20nM) with high selectivity against related FAD dependent aminoxidases (MAO-A/B, IL4I1, KDM1B >100uM, SMOX 7uM). Treatment of THP-1 (MLL-AF9) cells with ORY-1001, results in a time/dose dependent me2H3K4 accumulation a

FD1024 is a potent PIM inhibitor, displaying inhibitory concentrations (IC50s) of 1.96 nM, 38.9 nM, and 4.17 nM for PIM1, PIM2, and PIM3, respectively. It demonstrates significant antiproliferative effects on several AML cell lines, with IC50 values of 0.16 μM for EOL-1, 0.12 μM for MV-4-11, 1.05 μM for KG-1, and 1.39 μM for MOLM-16. Additionally, FD1024 has shown antitumor efficacy in murine models [1].

GNE-207 is a selective and orally bioavailable inhibitor of the bromodomain of CBP (IC50: 1 nM). It has a selective index of >2500-fold against BRD4 (1). GNE-207 displays excellent CBP potency (EC50: 18 nM for MYC expression in MV-4-11 cells).

PROTAC BRD4 Degrader-17 (compound 13i), a potent inhibitor, exhibits IC50 values of 29.54 nM (BRD4 (BD1)) and 3.82 nM (BRD4 (BD2)), effectively reducing Cyclin B1 expression linked with G2 M phase progression and significantly inducing apoptosis in MV-4-11 cells [1].

SNIPER(ABL)-015, a compound that conjugates GNF5 (ABL inhibitor) to MV-1 (IAP ligand) via a linker, effectively reduces BCR-ABL protein levels with a DC50 of 5 μM [1].

Compound 18, also known as FLT3/CHK-IN-1, is a dual inhibitor targeting FLT3 and CHK1, exhibiting over 1700-fold selectivity towards c-KIT and significantly diminishing hERG affinity, with an IC50 of 58.4 μM. It demonstrates efficacy in suppressing tumor growth in mouse xenotransplantation models implanted with MV-4-11 cells [1].

PROTAC BRD4 Degrader-16 is a potent degrader of BRD4, with IC50 values of 34.58 nM for BRD4 (BD1) and 40.23 nM for BRD4 (BD2). It significantly reduces Cyclin B1 expression, impedes G2 M phase progression, and induces apoptosis in MV-4-11 cells [1].

Antiproliferative agent-30 (Compound 8g) exhibits broad-spectrum antiproliferative activity, with IC50 values of 0.054 nM, 0.008 nM, and 0.144 nM against HCT-116, K562, and MV-4-11 cancer cell lines, respectively. It inhibits tubulin assembly, FLT3, and Abl1 kinases and shows vascular-disrupting capabilities. Additionally, it displays an anticancer effect against acute myeloid leukemia (AML) with FLT3-ITD-TKD mutations [1].

17R(18S)-EpETE is an oxylipin and a cytochrome P450 metabolite of eicosapentaenoic acid .1,217R(18S)-EpETE is an activator of large-conductance calcium-activated potassium (BKCa) channels, increasing the potassium current amplitude by 15-fold in isolated rat cerebral artery vascular smooth muscle cells (VSMCs) at +60 mV when used at a concentration of 50 nM.2It has negative chronotropic effects in isolated neonatal rat cardiomyocytes (NRCMs; EC50= ~1-2 nM) and prevents calcium-induced increases in the spontaneous beating of NRCMs.3,4 1.Schwarz, D., Kisselev, P., Ericksen, S.S., et al.Arachidonic and eicosapentaenoic acid metabolism by human CYP1A1: Highly steroselective formation of 17(R), 18(S)-epoxyeicosatetraenoic acidBiochem. Pharmacol.67(8)1445-1457(2004) 2.Lauterbach, B., Barbosa-Sicard, E., Wang, M.H., et al.Cytochrome P450-dependent eicosapentaenoic acid metabolites are novel BK channel activatorsHypertension39(2 Pt. 2)609-613(2002) 3.Falck, J.R., Wallukat, G., Puli, N., et al.17(R),18(S)-Epoxyeicosatetraenoic acid, a potent eicosapentaenoic acid (EPA) derived regulator of cardiomyocyte contraction: Structure-activity relationships and stable analoguesJ. Med. Chem.54(12)4109-4118(2011) 4.Arnold, C., Markovic, M., Blossey, K., et al.Arachidonic acid-metabolizing cytochrome P450 enzymes are targets of omega-3 fatty acidsJ. Biol. Chem.285(43)32720-32733(2010)

Quinine hemisulfate hydrate, an alkaloid extracted from the cinchona tree bark, serves as an anti-malarial agent and potassium channel inhibitor. It specifically targets and inhibits WT mouse Slo3 (K Ca 5.1) channel currents induced by voltage pulses to +100 mV, having an IC 50 value of 169 μM [1] [2].

Ebio1, a selective activator of the voltage-gated potassium channel KCNQ2, enhances channel conductance by promoting the formation of an expanded gate at a saturation voltage of +50 mV, leading to increased channel activity [1].

PROTAC ATR degrader-2 (Compound 8i) serves as a PROTAC degrader targeting ATR, effectively degrading it in acute myeloid leukemia (AML) cell lines MV-4-11 and MOLM-13, with DC50 values of 22.9 and 34.5 nM, respectively. This compound induces apoptosis and inhibits the proliferation of AML cells. Additionally, PROTAC ATR degrader-2 demonstrates favorable pharmacokinetic properties and potent antitumor activity in a mouse model of AML. (Pink: ATR ligand; Blue: E3 ligase ligand Lenalidomide; Black: linker) [1]

FLT3-IN-21 (compound LC-3), a potent FLT3 inhibitor with an IC50 value of 8.4 nM, induces apoptosis, arrests the cell cycle in the G1 phase, and effectively inhibits the proliferation of FLT3-ITD-positive AML cells MV-4-11 with an IC50 of 5.3 nM. In murine models, a daily dose of 10 mg kg FLT3-IN-21 markedly inhibited tumor growth in the MV-4-11 xenograft model, achieving a tumor growth inhibition (TGI) of 92.16% [1].

SNIPER(ABL)-047, a compound that links HG-7-85-01 (an ABL inhibitor) to MV-1 (an IAP ligand) via a linker, effectively decreases the BCR-ABL protein levels, achieving a DC50 value of 2 μM[1].

SNIPER(ABL)-050 is a chemical compound that combines Imatinib, an ABL inhibitor, with MV-1, an IAP ligand, using a linker. This conjugation results in the reduction of BCR-ABL protein[1].

SNIPER(ABL)-019, a compound that links Dasatinib (ABL inhibitor) to MV-1 (IAP ligand) via a linker, effectively reduces BCR-ABL protein levels, exhibiting a DC50 of 0.3 μM[1].

Quinidine is a potent, orally active, selective inhibitor of cytochrome P450db. Quinidine hydrobromide is a K + channel blocker (IC 50= 19.9 μM). Quinidine hydrobromide shows antiarrhythmic activity. Quinidine hydrobromide can be used for malaria research.

Quinine sulfate dihydrate plays a major role in potassium channel blockers. It is also used as an antimalarial, anticholinergic, antihypertensive and a hypoglycemic agent. It inhibits mitochondrial ATP-regulated potassium channel. It is also used to study the metabolism of biocrystalized heme, hemozoin, in malarial parasites and to study the toxicity of heme (FP)-complexes.

Quinine is a natural cinchona alkaloid that has been used for centuries in the prevention and therapy of malaria. Quinine is also used for idiopathic muscle cramps. Quinine therapy has been associated with rare instances of hypersensitivity reactions which can be accompanied by hepatitis and mild jaundice.

Quinine hydrochloride dihydrate (Quinine HCl Dihydrate) is a white crystalline K+ channel blocker, used to treat malaria.

Quinidine is an antiarrhythmic agent. Quinidine is a potent, orally active, selective cytochrome P450db inhibitor. Quinidine is also a blocker of K + channel with an IC 50 of 19.9 μM. Quinidine has potential to be used for malaria research [1] [2] [3].

Quinine dihydrochloride (Quinine bimuriate) is a primary alkaloid of various species of Cinchona (Rubiaceae). It is also an antimalarial and muscle relaxant (skeletal).