l 30

L 30 is a blocker of the sodium channel.

Iptacopan (LNP023) is an inhibitor with high affinity to factor B, with a KD value of 7.9 nM and an IC50 value of 10 nM.

L-161240 is an antimicrobial agent associated with lipid A biosynthesis with an IC50 value of 30 nM as determined by DEACET and a MIC value of 1-3 μg mL against wild-type E. coli.

MK-886 (L 663536) is an inhibitor of leukotriene biosynthesis, acting by inhibiting the 5-lipoxygenase-activating protein (FLAP), and serves as a moderately potent PPARα antagonist.

L-779450, an effective, ATP-competitive Raf kinase inhibitor (IC50: 10 nM) , displays > 7, > 30 and > 70-fold selectivity over p38α, GSK3β and Lck respectively.

Compound 17k, also known as Antileishmanial agent-30, effectively inhibits Leishmania with an IC50 of 0.2 μM for L. donovani. It exhibits a CC50 of >100 μM and an SI of >500, indicating significant selectivity and potency.

β-Defensin-3 is a peptide with antimicrobial properties that protects the skin and mucosal membranes of the respiratory, genitourinary, and gastrointestinal tracts. It inhibits the growth of the periodontopathogenic and cariogenic bacteria F. nucleatum, S. mutans, S. sobrinus, S. salivarius, and L. casei (MICs = 12.5-100 mg/l). It also inhibits the growth of S. aureus, S. pyogenes, P. aeruginosa, E. coli, and C. albicans. β-Defensin-3 stimulates gene expression and production of IL-6, IL-10, CXCL10, CCL2, MIP-3α, and RANTES by keratinocytes when used at a concentration of 30 μg/ml. It also stimulates calcium mobilization, migration, and proliferation of keratinocytes when used at concentrations of 30, 5, and 20 μg/ml, respectively. β-Defensin-3 induces IL-31 production by human peripheral blood-derived mast cells in vitro when used at a concentration of 10 μg/ml and by rat mast cells in vivo following a 500 ng intradermal dose.

Palmitic acid-13C (C1, C2, C3, and C4 labeled) is intended for use as an internal standard for the quantification of palmitic acid by GC- or LC-MS. Palmitic acid is a common 16-carbon saturated fat that represents 10-20% of human dietary fat intake and comprises approximately 25 and 65% of human total plasma lipids and saturated fatty acids, respectively.1,2Acylation of palmitic acid to proteins facilitates anchoring of membrane-bound proteins to the lipid bilayer and trafficking of intracellular proteins, promotes protein-vesicle interactions, and regulates various G protein-coupled receptor functions.1Red blood cell palmitic acid levels are increased in patients with metabolic syndrome compared to patients without metabolic syndrome and are also increased in the plasma of patients with type 2 diabetes compared to individuals without diabetes.3,4 1.Fatima, S., Hu, X., Gong, R.-H., et al.Palmitic acid is an intracellular signaling molecule involved in disease developmentCell. Mol. Life Sci.76(13)2547-2557(2019) 2.Santos, M.J., López-Jurado, M., Llopis, J., et al.Influence of dietary supplementation with fish oil on plasma fatty acid composition in coronary heart disease patientsAnn. Nutr. Metab.39(1)52-62(1995) 3.Yi, L.-Z., He, J., Liang, Y.-Z., et al.Plasma fatty acid metabolic profiling and biomarkers of type 2 diabetes mellitus based on GC/MS and PLS-LDAFEBS Lett.580(30)6837-6845(2006) 4.Kabagambe, E.K., Tsai, M.Y., Hopkins, P.N., et al.Erythrocyte fatty acid composition and the metabolic syndrome: A National Heart, Lung, and Blood Institute GOLDN studyClin. Chem.54(1)154-162(2008)

CC-90005 is a potent, selective, and orally active inhibitor of protein kinase C-θ (PKC-θ) with an IC50 of 8 nM, demonstrating strong selectivity over PKC-δ (IC50=4440 nM). Additionally, CC-90005 can inhibit T cell activation by IL-2 expression[1].

Diallyl tetrasulfide is an organosulfur compound that has been found in A. sativum and has diverse biological activities, including antimicrobial, antioxidant, and anticancer properties.[1],[2],[3],[4] It is active against the bacteria S. aureus and methicillin-resistant S. aureus (MRSA; MICs = 0.5 and 2 mg/L, respectively), as well as the fungi C. albicans, C. krusei, C. glabrata, A. niger, A. flavus, and A. fumigatus (MICs = 0.5, 4, 2, 1, 2, and 4 mg/L, respectively).[1] It reduces cadmium-induced increases in hepatic levels of thiobarbituric acid reactive substances (TBARS) and increases cadmium-induced decreases in the hepatic activity of superoxide dismutase (SOD1), catalase, GST, and glucose-6-phosphate dehydrogenase (G6PDH) in rats when administered at a dose of 40 mg/kg.[2] Diallyl tetrasulfide is cytotoxic to MCF-7 breast cancer cells (IC50 = 92 μM) and reduces tumor growth in a BGC-823 mouse xenograft model when administered at doses of 20, 30, and 40 mg/kg for 32 days.[3],[4]

C8 L-threo Ceramide is a bioactive sphingolipid and cell-permeable analog of naturally occurring ceramides. It is cytotoxic to U937 cells (IC50 = 10 μM) and, like C8 D-threo ceramide , induces nuclear DNA fragmentation 5- to 6-fold more potently than C8 L-erythro ceramide . C8 D-threo Ceramide also enhances V. cholerae cytolysin pore formation in liposome lipid membranes, as measured by calcein release, with a 50% release dose (RD50) value of ~30 μg ml.

Pestalotin is a fungal metabolite originally isolated from P. cryptomeriaecola with diverse biological activities. It induces reducing sugar release in embryoless rice endosperms when used at concentrations ranging from 3 to 100 mg L and enhances growth of rice seedlings (O. sativa) when used in combination with gibberellin A3 at concentrations ranging from 30 to 500 mg L. Pestalotin has antifungal activity, reducing the growth of C. albicans, C. neoformans, T. rubrum, and A. fumigatus (MICs = 12.5, 50, 50, and 50 μg ml, respectively). It is cytotoxic to HL-60, MKN45, LoVo, and A549 cells (IC50s = 64.87-182.92 μM). Pestalotin has been used as a standard for dereplication of natural products.

Ara-G is an analog of the nucleoside guanosine and an active metabolite of nelarabine .1,2 Ara-G accumulates in T lymphoblasts and malignant T-lymphoid cells, where it is phosphorylated to produce ara-GTP and incorporated into the DNA.3,1 Ara-G inhibits DNA replication by 92% after 30 minutes when used at a concentration of 50 μM in CEM cells, which are used as a model for human T lymphoblasts.1 It also halts the cell cycle at the sub-G1 phase and induces apoptosis in CEM cells.3 Syngeneic bone marrow containing 6C3HED tumor cells treated with ara-G (100 mM) ex vivo prior to transplantation increases survival of lethally irradiated mice and induces reconstitution of lymphoid, myeloid, and erythroid cell linages.4References1. Leanza, L., Miazzi, C., Ferraro, P., et al. Activation of guanine-β-D-arabinofuranoside and deoxyguanosine to triphosphates by a common pathway blocks T lymphoblasts at different checkpoints. Exp. Cell Res. 316(20), 3443-3453 (2010).2. Lambe, C.U., Averett, D.R., Paff, M.T., et al. 2-Amino-6-methoxypurine arabinoside: An agent for T-cell malignancies. Cancer Res. 55(15), 3352-3356 (1995).3. Rodriguez, C.O., Jr., Stellrecht, C.M., and Gandhi, V. Mechanisms for T-cell selective cytotoxicity of arabinosylguanine. Blood 102(5), 1842-1848 (2003).4. Kurtzberg, J. Guanine arabinoside as a bone marrow-purging agent. Ann. N.Y. Acad. Sci 685(1), 225-236 (1993). Ara-G is an analog of the nucleoside guanosine and an active metabolite of nelarabine .1,2 Ara-G accumulates in T lymphoblasts and malignant T-lymphoid cells, where it is phosphorylated to produce ara-GTP and incorporated into the DNA.3,1 Ara-G inhibits DNA replication by 92% after 30 minutes when used at a concentration of 50 μM in CEM cells, which are used as a model for human T lymphoblasts.1 It also halts the cell cycle at the sub-G1 phase and induces apoptosis in CEM cells.3 Syngeneic bone marrow containing 6C3HED tumor cells treated with ara-G (100 mM) ex vivo prior to transplantation increases survival of lethally irradiated mice and induces reconstitution of lymphoid, myeloid, and erythroid cell linages.4 References1. Leanza, L., Miazzi, C., Ferraro, P., et al. Activation of guanine-β-D-arabinofuranoside and deoxyguanosine to triphosphates by a common pathway blocks T lymphoblasts at different checkpoints. Exp. Cell Res. 316(20), 3443-3453 (2010).2. Lambe, C.U., Averett, D.R., Paff, M.T., et al. 2-Amino-6-methoxypurine arabinoside: An agent for T-cell malignancies. Cancer Res. 55(15), 3352-3356 (1995).3. Rodriguez, C.O., Jr., Stellrecht, C.M., and Gandhi, V. Mechanisms for T-cell selective cytotoxicity of arabinosylguanine. Blood 102(5), 1842-1848 (2003).4. Kurtzberg, J. Guanine arabinoside as a bone marrow-purging agent. Ann. N.Y. Acad. Sci 685(1), 225-236 (1993).

L-AP4 (L-APB) monohydrate is a potent and specific agonist for group III mGluRs, with EC50s of 0.13, 0.29, 1.0, and 249 μM for mGlu4, mGlu8, mGlu6, and mGlu7 receptors, respectively [1][2].

Avilamycin A is an antibiotic.1 It is active against veterinary isolates of C. perfringens (MICs = ≤0.06-0.5 mg/L) and B. hyodysenteriae (MICs = 12.5-100 μg/ml).1,2 Dietary administration of avilamycin A (15 and 30 ppm) reduces mortality in a broiler cockerel model of C. perfringens infection.3 Formulations containing avilamycin A have been used in the prevention of necrotic enteritis in livestock. |1. Watkins, K.L., Shryock, T.R., Dearth, R.N., et al. In-vitro antimicrobial susceptibility of Clostridium perfringens from commercial turkey and broiler chicken origin. Vet. Microbiol. 54(2), 195-200 (1997).|2. Uezato, K., Kinjo, E., and Adachi, Y. In vitro susceptibility of 21 antimicrobial agents to 37 isolates of Brachyspira hyodysenteriae isolated from pigs in Okinawa Prefecture. J. Vet. Med. Sci. 66(3), 307-309 (2004).|3. Paradis, M.A., McMillan, E., Bagg, R., et al. Efficacy of avilamycin for the prevention of necrotic enteritis caused by a pathogenic strain of Clostridium perfringens in broiler chickens. Avian Pathol. 45(3), 365-369 (2016).

Rec 15/2615 is an antagonist of α1B-adrenergic receptors (α1B-ARs; Ki = 0.45 nM for the recombinant human receptor).1 It selectively inhibits α1B-ARs over α1A-, α1D-, and α1L-ARs (Kis = 7.59, 10.23, and 49 nM, respectively). Rec 15/2615 inhibits norepinephrine-induced contractions of isolated rabbit prostate and urethral strips (Kis = 100 and 316.2 nM, respectively), as well as reduces norepinephrine-induced contractions of chloroethylclonidine-precontracted isolated rabbit aortic rings (Ki = 50 nM).2 It decreases diastolic blood pressure (ED25 = 183 μg/kg, i.v.) and increases intracavernous pressure in anesthetized dogs when administered intracavernously at doses ranging from 30 and 1,000 μg/kg.1,2 |1. Sironi, G., Colombo, D., Poggesi, E., et al. Effects of intracavernous administration of selective antagonists of α1-adrenoceptor subtypes on erection in anesthetized rats and dogs. J. Pharmacol. Exp. Ther. 292(3), 974-981 (2000).|2. Testa, R., Guarneri, L., Angelico, P., et al. Pharmacological characterization of the uroselective alpha-1 antagonist Rec 15/2739 (SB 216469): Role of the alpha-1L adrenoceptor in tissue selectivity, part II. J. Pharmacol. Exp. Ther. 281(3), 1284-1293 (1997).

CP-609754 (LNK-754) is a potent and reversible farnesyltransferase inhibitor with potential anticancer activity. It inhibits farnesylation of recombinant human H-Ras (IC50=0.57 ng mL) and K-Ras (IC50=46 ng mL)[1]. In 3T3 H-ras (61L)-transfected cell lines, CP-609754 exhibits a slow on off rate, inhibiting mutant H-Ras farnesylation with an IC50 of 1.72 ng mL[1]. The compound is competitive for the prenyl acceptor (H-Ras protein) and noncompetitive for the prenyl donor farnesyl PPI, selectively inhibiting farnesylation of both H- and K-Ras proteins in 3T3 transfectants[1]. In vivo, CP-609754 shows antitumor activity against 3T3 H-ras (61L) tumors, with tumor regression achieved at 100 mg kg twice daily and an ED50 for tumor growth inhibition at 28 mg kg[1]. Continuous i.p. infusion of CP-609754 inhibits tumor growth by over 50% and reduces tumor farnesyltransferase activity by over 30% when plasma concentration is maintained above 118 ng mL[1]. [1]. Stacy L Moulder, et al. A phase I open label study of the farnesyltransferase inhibitor CP-609,754 in patients with advanced malignant tumors. Clin Cancer Res. 2004 Nov 1;10(21):7127-35.

Ribavirin-13C5is intended for use as an internal standard for the quantification of ribavirin by GC- or LC-MS. Ribavirin is an antiviral guanosine nucleoside analog.1,2Upon entry into cells, ribavirin is metabolized to an active triphosphate form that induces viral RNA chain termination and inhibits viral polymerases. It reduces replication in a panel of seven RNA and four DNA viruses in Vero cells (EC50s = 2-95 μg/ml).3Ribavirin also reduces replication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in Vero cells (EC50= 109.5 μM).4Aerosol administration of ribavirin (30 mg/kg) reduces mortality in a mouse model of influenza A infection.5Formulations containing ribavirin have been used in the treatment of respiratory syncytial virus (RSV), hepatitis C virus (HCV), and viral hemorrhagic fevers. 1.Gilbert, B.E., and Knight, V.Biochemistry and clinical applications of ribavirinAntimicrob. Agents Chemother.30(2)201-205(1986) 2.Gordon, C.J., Tchesnokov, E.P., Woolner, E., et al.Remdesivir is a direct-acting antiviral that inhibits RNA-dependent RNA polymerase from severe acute respiratory syndrome coronavirus 2 with high potencyJ. Biol. Chem.295(20)6785-6797(2020) 3.Kirsi, J.J., North, J.A., McKernan, P.A., et al.Broad-spectrum antiviral activity of 2-β-D-ribofuranosylselenazole-4-carboxamide, a new antiviral agentAntimicrob. Agents Chemother.24(3)353-361(1983) 4.Wang, M., Cao, R., Zhang, L., et al.Remdesivir and chloroquine effectively inhibit the recently emerged novel coronavirus (2019-nCoV) in vitroCell Res.30(3)269-271(2020) 5.Wilson, S.Z., Knight, V., Wyde, P.R., et al.Amantadine and ribavirin aerosol treatment of influenza A and B infection in miceAntimicrob. Agents Chemother.17(4)642-648(1980)

CU-32 is an inhibitor of cyclic GMP-AMP (cGAMP) synthase (cGAS; IC50= 0.45 μM).1It reduces DNA-, but not Sendai virus-, induced dimerization of IFN regulatory factor 3 in THP-1 cells, indicating selectivity for the cGAS DNA sensing pathway over the RIG-I-MAVS RNA sensing pathway. It is also selective for cGAS over toll-like receptors (TLRs) at 50 μM. CU-32 decreases IFN-stimulatory DNA-induced production of IFN-β in THP-1 cells when used at concentrations of 10, 30, and 100 μM. 1.Padilla-Salinas, R., Sun, L., Anderson, R., et al.Discovery of small-molecule cyclic GMP-AMP synthase inhibitorsJ. Org. Chem.85(3)1579-1600(2020)

CU-76 is an inhibitor of cyclic GMP-AMP synthase (cGAS; IC50= 0.24 μM).1It reduces DNA-, but not Sendai virus-, induced dimerization of IFN regulatory factor 3 in THP-1 cells, indicating selectivity for the cGAS DNA sensing pathway over the RIG-I-MAVS RNA sensing pathway. CU-76 decreases IFN-stimulatory DNA-induced production of IFN-β in THP-1 cells when used at concentrations of 10, 30, and 100 μM. 1.Padilla-Salinas, R., Sun, L., Anderson, R., et al.Discovery of small-molecule cyclic GMP-AMP synthase inhibitorsJ. Org. Chem.85(3)1579-1600(2020)

TAS 205 is an inhibitor of hematopoietic prostaglandin D synthase (H-PGDS; IC50= 55.8 nM).1It is selective for H-PGDS over lipocalin-type PGDS (L-PGDS) at 100 μM, as well as over enzyme and receptor panels at 10 μM. TAS 205 inhibits production of prostaglandin D2induced by A23187 in KU812 human and RBL-2H3 rat basophils with IC50values of 78.3 and 181.3 nM, respectively. It inhibits ovalbumin-induced nasal lavage fluid eosinophil infiltration and late-phase nasal obstruction in an ovalbumin-sensitized guinea pig model of allergic rhinitis when administered at a dose of 30 mg/kg. 1.Aoyagi, H., Kajiwara, D., Tsunekuni, K., et al.Potential synergistic effects of novel hematopoietic prostaglandin D synthase inhibitor TAS-205 and different types of anti-allergic medicine on nasal obstruction in a Guinea pig model of experimental allergic rhinitisEur. J. Pharmacol.875173030(2020)

Methyl cis-4-Hydroxy-L-proline Hydrochloride is a useful organic compound for research related to life sciences. The catalog number is T65222 and the CAS number is 40126-30-5.

L-Afegostat (5-epi-Isofagomine), a glycosidase inhibitor and an iminosugar, is utilized in carbohydrate synthesis. It demonstrates β-Glucosidase inhibition with a Ki of 30 μM.

ω-Agatoxin IVA TFA is a potent selective inhibitor of P Q type Ca2+ (Cav2.1) channels, with IC50 values of 2 nM for P-type and 90 nM for Q-type channels. It effectively inhibits glutamate exocytosis and calcium influx induced by high potassium, with IC50 values ranging from 30 to 225 nM. Additionally, it blocks high potassium-induced serotonin and norepinephrine release, without impacting L-type or N-type calcium channels [1][2].