m-25

M-25 is a Smoothened antagonist and inhibitor of the Hedgehog pathway.

M 25 is a Smoothened (Smo) receptor antagonist.

Alvameline maleate is used as a Partial M1 Agonist and M2/M3 Antagonist.

AZD-8529 mesylate is a highly selective, and orally bioavailable positive allosteric modulator of mGluR2 (EC50: 285 nM). It shows no positive allosteric modulator responses at 20-25 M on the mGluR1, 3, 4, 5, 6, 7, and 8 subtypes.

Myrothecine A, a trichothecene mycotoxin discovered in M. roridum, exhibits anticancer properties. It effectively inhibits the proliferation of various cancer cell lines, specifically A549, MCF-7, HepG2, and SMMC-7721, with IC50 values of 95, 70, 60, and 25 µM, respectively. At a concentration of 50 µM, Myrothecine A induces G1 cell cycle arrest in HepG2 cells and promotes apoptosis in SMMC-7721 cells by elevating levels of Bax and cleaved caspase-3, -5, and -8.

Urocortin II is a neuropeptide hormone and member of the corticotropin-releasing factor (CRF) family which includes mammalian CRF , urocortin , urocortin III , frog sauvagine, and piscine urotensin I.1 Mouse urocortin II shares 34 and 42% sequence homology with rat CRF and urocortin . It is expressed in mouse paraventricular, supraoptic, and arcuate nuclei of the hypothalamus, the locus coeruleus, and in motor nuclei of the brainstem and spinal ventral horn. Urocortin II selectively binds to CRF1 over CRF2 receptors (Kis = 0.66 and >100 nM, respectively) and induces cAMP production in CHO cells expressing CRF2 (EC50 = 0.14 nM). In vivo, urocortin II suppresses nighttime food intake by 35% in rats when administered intracerebroventricularly at a dose of 1 μg. Urocortin II (0.1 and 0.5 μg, i.c.v) stimulates fecal pellet output, increases distal colonic transit, and inhibits gastric emptying in mice.2References1. Reyes, T.M., Lewis, K., Perrin, M.H., et al. Urocortin II: A member of the corticotropin-releasing factor (CRF) neuropeptide family that is selectively bound by type 2 CRF receptors. Proc. Natl. Acad. Sci. U.S.A. 98(5), 2843-2848 (2001).2. Martinez, V., Wang, L., Million, M., et al. Urocortins and the regulation of gastrointestinal motor function and visceral pain. Peptides 25(10), 1733-1744 (2004). Urocortin II is a neuropeptide hormone and member of the corticotropin-releasing factor (CRF) family which includes mammalian CRF , urocortin , urocortin III , frog sauvagine, and piscine urotensin I.1 Mouse urocortin II shares 34 and 42% sequence homology with rat CRF and urocortin . It is expressed in mouse paraventricular, supraoptic, and arcuate nuclei of the hypothalamus, the locus coeruleus, and in motor nuclei of the brainstem and spinal ventral horn. Urocortin II selectively binds to CRF1 over CRF2 receptors (Kis = 0.66 and >100 nM, respectively) and induces cAMP production in CHO cells expressing CRF2 (EC50 = 0.14 nM). In vivo, urocortin II suppresses nighttime food intake by 35% in rats when administered intracerebroventricularly at a dose of 1 μg. Urocortin II (0.1 and 0.5 μg, i.c.v) stimulates fecal pellet output, increases distal colonic transit, and inhibits gastric emptying in mice.2 References1. Reyes, T.M., Lewis, K., Perrin, M.H., et al. Urocortin II: A member of the corticotropin-releasing factor (CRF) neuropeptide family that is selectively bound by type 2 CRF receptors. Proc. Natl. Acad. Sci. U.S.A. 98(5), 2843-2848 (2001).2. Martinez, V., Wang, L., Million, M., et al. Urocortins and the regulation of gastrointestinal motor function and visceral pain. Peptides 25(10), 1733-1744 (2004).

Monascuspiloin is a fungal metabolite that has been found inM. pilosusM93-fermented rice.1It induces endoplasmic reticulum stress and autophagy in PC3 prostate cancer cells. Monascuspiloin (15-45 μM) decreases viability of PC3 cells and has an additive effect on the reduction in viability of PC3 cells induced by irradiation when used at a concentration of 25 μM. It induces intratumor apoptosis and autophagy and reduces tumor growth in a PC3 mouse xenograft model when administered at doses of 40 and 120 mg/kg.2 1.Chiu, H.-W., Fang, W.-H., Chen, Y.-L., et al.Monascuspiloin enhances the radiation sensitivity of human prostate cancer cells by stimulating endoplasmic reticulum stress and inducing autophagyPLoS One7(7)e40462(2012) 2.Chen, R.-J., Hung, C.-M., Chen, Y.-L., et al.Monascuspiloin induces apoptosis and autophagic cell death in human prostate cancer cells via the Akt and AMPK signaling pathwaysJ. Agric. Food Chem.60(29)7185-7193(2012)

6,9-Dichloro-1,2,3,4-tetrahydroacridine is a synthetic intermediate in the synthesis of tacrine-based acetylcholinesterase (AChE) inhibitors.1It is also an intermediate in the synthesis of multifunctional tacrine hybrids that possess radical scavenging, amyloid-β aggregation inhibitory, and/or β-secretase 1 (BACE1) inhibitory activities in addition to their activity as AChE inhibitors.2,3 1.Recanatini, M., Cavalli, A., Belluti, F., et al.SAR of 9-amino-1,2,3,4-tetrahydroacridine-based acetylcholinesterase inhibitors: Synthesis, enzyme inhibitory activity, QSAR, and structure-based CoMFA of tacrine analoguesJ. Med. Chem.43(10)2007-2018(2000) 2.Digiacomo, M., Chen, Z., Wang, S., et al.Synthesis and pharmacological evaluation of multifunctional tacrine derivatives against several disease pathways of ADBioorg. Med. Chem. Lett.25(4)807-810(2015) 3.Li, S.Y., Jiang, N., Xie, S.S., et al.Design, synthesis and evaluation of novel tacrine-rhein hybrids as multifunctional agents for the treatment of Alzheimer's diseaseOrg. Biomol. Chem.12(5)801-814(2014)

m-PEG25-Propargyl, a PEG-based linker for PROTACs, joins two essential ligands crucial for forming PROTAC molecules and enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

α-Melanocyte-stimulating hormone (α-MSH) is a 13-amino acid peptide hormone produced by post-translational processing of proopiomelanocortin (POMC) in the pituitary gland, as well as in keratinocytes, astrocytes, monocytes, and gastrointestinal cells.1It is an agonist of melanocortin receptor 3 (MC3R) and MC4R that induces cAMP production in Hepa cells expressing the human receptors (EC50s = 0.16 and 56 nM, respectively).2α-MSH (100 pM) reducesS. aureuscolony formation andC. albicansgerm tube formationin vitro.3It inhibits endotoxin-, ceramide-, TNF-α-, or okadaic acid-induced activation of NF-κB in U937 cells.1α-MSH reduces IL-6- or TNF-α-induced ear edema in mice.4It also prevents the development of adjuvant-induced arthritis in rats and increases survival in a mouse model of septic shock. Increased plasma levels of α-MSH are positively correlated with delayed disease progression and reduced death in patients with HIV.1 1.Catania, A., Airaghi, L., Colombo, G., et al.α-melanocyte-stimulating hormone in normal human physiology and disease statesTrends Endocrinol. Metab.11(8)304-308(2000) 2.Miwa, H., Gantz, I., Konda, Y., et al.Structural determinants of the melanocortin peptides required for activation of melanocortin-3 and melanocortin-4 receptorsJ. Pharmacol. Exp. Ther.273(1)367-372(1995) 3.Cutuli, M., Cristiani, S., Lipton, J.M., et al.Antimicrobial effects of a-MSH peptidesJ. Leukoc. Biol.67(2)233-239(2000) 4.Lipton, J.M., Ceriani, G., Macaluso, A., et al.Antiiinflammatory effect of the neuropeptide a-MSH in acute, chronic, and systemic inflammationAnn. N.Y. Acad. Sci.25(741)137-148(1994)

Palmitic acid-13C is intended for use as an internal standard for the quantification of palmitic acid by GC- or LC-MS. Palmitic acid is a 16-carbon saturated fatty acid. It comprises approximately 25% of human total plasma lipids.1 It increases protein levels of COX-2 in RAW 264.7 cells when used at a concentration of 75 μM.2 Palmitic acid is involved in the acylation of proteins to anchor membrane-bound proteins to the lipid bilayer.2,3,4,5,6 |1. 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 patients. Ann. Nutr. Metab. 39(1), 52-62 (1995).|2. Lee, J.Y., Sohn, K.H., Rhee, S.H., et al. Saturated fatty acids, but not unsaturated fatty acids, induced the expression of cyclooxygenase-2 mediated through toll-like receptor 4. J. Biol. Chem. 276(20), 16683-16689 (2001).|3. Dietzen, D.J., Hastings, W.R., and Lublin, D.M. Caveolin is palmitoylated on multiple cysteine residues. Palmitoylation is not necessary for localization of caveolin to caveolae. J. Biol. Chem. 270(12), 6838-6842 (1995).|4. Robinson, L.J., and Michel, T. Mutagenesis of palmitoylation sites in endothelial nitric oxide synthase identifies a novel motif for dual acylation and subcellular targeting. Proc. Nat. Acad. Sci. USA 92(25), 11776-11780 (1995).|5. Topinka, J.R., and Bredt, D.S. N-terminal palmitoylation of PSD-95 regulates association with cell membranes and interaction with K+ channel Kv1.4. Neuron 20(1), 125-134 (1998).|6. Miggin, S.M., Lawler, O.A., and Kinsella, B.T. Palmitoylation of the human prostacyclin receptor. Functional implications of palmitoylation and isoprenylation. J. Biol. Chem. 278(9), 6947-6958 (2003).

Pyrenocine A is a fungal metabolite that has been found inP. terrestrisand has diverse biological activities.1It inhibits the asexual spore germination of the plant pathogenic fungiF. oxysporum,F. solani,M. hiemalis, andR. stolonifer(EC50s = 14, 20, 20, and 25 μg/ml, respectively). Pyrenocine A is active againstB. subtilis,S. aureus, andE. coli(IC50s = 30, 45, and 200 μg/ml, respectively). It inhibits onion seedling elongation (EC50= 4 μg/ml). Pyrenocine A is also a phytotoxin that inhibits lettuce seed germination and rice seedling elongation.2,3 1.Sparace, S.A., Reeleder, R.D., and Khanizadeh, S.Antibiotic activity of the pyrenocinesCan. J. Microbiol.33(4)327-330(1987) 2.Sato, H., Konoma, K., and Sakamura, S.Phytotoxins produced by onion pink root fungus, Pyrenochaeta terrestrisAgric. BioI. Chem.43(11)2409-2411(1979) 3.Sato, H., Konoma, K., Sakamura, S., et al.X-Ray crystal structure of pyrenocine A, a phytotoxin from Pyrenochaeta terrestrisAgric. BioI. Chem.45(3)795-797(1981)

NG 25 is a type II kinase inhibitor that inhibits MAP4K2 and TAK1 (IC50s = 21.7 and 149 nM, respectively).1It also inhibits the Src family kinases Src and LYN (IC50s = 113 and 12.9 nM, respectively) and Abl family kinases (IC50s = 75.2 nM), as well as CSK, FER, and p38α (IC50s = 56.4, 82.3, and 102 nM, respectively). NG 25 (100 nM) prevents TNF-α-induced IKKα/β phosphorylation and IκB-α degradation in L929 cells. It inhibits secretion of IFN-α and IFN-β induced by CpG type B and CL097, respectively, in Gen2.2 cells in a concentration-dependent manner.2NG 25 decreases cell viability of HCT116KRASWT, and to a greater degree of HCT116KRASG13D, colorectal cancer cells in a concentration-dependent manner.3It also reduces tumor growth and increases the number of TUNEL-positive tumor cells in a CT26KRASG12Dmouse orthotopic model of colorectal cancer. 1.Tan, L., Nomanbhoy, T., Gurbani, D., et al.Discovery of type II inhibitors of TGFβ-activated kinase 1 (TAK1) and mitogen-activated protein kinase kinase kinase kinase 2 (MAP4K2)J. Med. Chem.58(1)183-196(2015) 2.Pauls, E., Shpiro, N., Peggie, M., et al.Essential role for IKKβ in production of type 1 interferons by plasmacytoid dendritic cellsJ. Biol. Chem. 287(23)19216-19228(2012) 3.Ma, Q., Gu, L., Liao, S., et al.NG25, a novel inhibitor of TAK1, suppresses KRAS-mutant colorectal cancer growth in vitro and in vivoApoptosis24(1-2)83-94(2019)

Urocortin III is a neuropeptide hormone and member of the corticotropin-releasing factor (CRF) family which includes mammalian CRF , urocortin , urocortin II , frog sauvagine, and piscine urotensin I.1 Human urocortin III shares 90, 40, 37, and 21% identity to mouse urocortin III , mouse urocortin II , human urocortin , and mouse urocortin, respectively. Urocortin III selectively binds to type 2 CRF receptors (Kis = 21.7, 13.5, and >100 nM for rat CRF2α, rat CRF2β, and human CRF1, respectively). It stimulates cAMP production in CHO cells expressing rat CRF2α and mouse CRF2β (EC50s = 0.16 and 0.12 nM, respectively) as well as cultured anterior pituitary cells expressing endogenous CRF2β. Urocortin III is co-released with insulin to potentiate glucose-stimulated somatostatin release in vitro in human pancreatic β-cells.2 In vivo, urocortin III reduces food intake in a dose- and time-dependent manner in mice with a minimum effective dose (MED) of 0.3 nmol/animal.3 It increases swimming time in a forced swim test in mice, indicating antidepressant-like activity.4References1. Lewis, K., Li, C., Perrin, M.H., et al. Identification of urocortin III, an additional member of the corticotropin-releasing factor (CRF) family with high affinity for the CRF2 receptor. Proc. Natl. Acad. Sci. U.S.A. 98(13), 7570-7575 (2001).2. van der Meulen, T., Donaldson, C.J., Cáceres, E., et al. Urocortin3 mediates somatostatin-dependent negative feedback control of insulin secretion. Nat. Med. 21(7), 769-776 (2015).3. Pelleymounter, M.A., Joppa, M., Ling, N., et al. Behavioral and neuroendocrine effects of the selective CRF2 receptor agonists urocortin II and urocortin III. Peptides 25(4), 659-666 (2004).4. Tanaka, M., Kádár, K., Tóth, G., et al. Antidepressant-like effects of urocortin 3 fragments. Brain Res. Bull. 84(6), 414-418 (2011). Urocortin III is a neuropeptide hormone and member of the corticotropin-releasing factor (CRF) family which includes mammalian CRF , urocortin , urocortin II , frog sauvagine, and piscine urotensin I.1 Human urocortin III shares 90, 40, 37, and 21% identity to mouse urocortin III , mouse urocortin II , human urocortin , and mouse urocortin, respectively. Urocortin III selectively binds to type 2 CRF receptors (Kis = 21.7, 13.5, and >100 nM for rat CRF2α, rat CRF2β, and human CRF1, respectively). It stimulates cAMP production in CHO cells expressing rat CRF2α and mouse CRF2β (EC50s = 0.16 and 0.12 nM, respectively) as well as cultured anterior pituitary cells expressing endogenous CRF2β. Urocortin III is co-released with insulin to potentiate glucose-stimulated somatostatin release in vitro in human pancreatic β-cells.2 In vivo, urocortin III reduces food intake in a dose- and time-dependent manner in mice with a minimum effective dose (MED) of 0.3 nmol/animal.3 It increases swimming time in a forced swim test in mice, indicating antidepressant-like activity.4 References1. Lewis, K., Li, C., Perrin, M.H., et al. Identification of urocortin III, an additional member of the corticotropin-releasing factor (CRF) family with high affinity for the CRF2 receptor. Proc. Natl. Acad. Sci. U.S.A. 98(13), 7570-7575 (2001).2. van der Meulen, T., Donaldson, C.J., Cáceres, E., et al. Urocortin3 mediates somatostatin-dependent negative feedback control of insulin secretion. Nat. Med. 21(7), 769-776 (2015).3. Pelleymounter, M.A., Joppa, M., Ling, N., et al. Behavioral and neuroendocrine effects of the selective CRF2 receptor agonists urocortin II and urocortin III. Peptides 25(4), 659-666 (2004).4. Tanaka, M., Kádár, K., Tóth, G., et al. Antidepressant-like effects of urocortin 3 fragments. Brain Res. Bull. 84(6), 414-418 (2011).

TT15 is an agonist of the GLP-1R.

M‑89 is a Highly Potent Inhibitor of the Menin-Mixed Lineage Leukemia (Menin-MLL) Protein−Protein Interaction (Kd = 1.4 nM; IC50 = 25nM). M-89 binds to menin with a Kd value of 1.4 nM and effectively engages cellular menin protein at low nanomolar concentrations. M-89 inhibits cell growth in the MV4;11 and MOLM-13 leukemia cell lines carrying MLL fusion with IC50 values of 25 and 55 nM, respectively, and demonstrates >100-fold selectivity over the HL-60 leukemia cell line lacking MLL fusion.

AZD-8529 is a highly selective, and orally bioavailable positive allosteric modulator of mGluR2 (EC50: 285 nM). It shows no positive allosteric modulator responses at 20-25 M on the mGluR1, 3, 4, 5, 6, 7, and 8 subtypes.

Hirsutide is a cyclotetrapeptide fungal metabolite produced by the entomopathogenic fungus Hirsutella. It has antibacterial activity against C. pyogenes, S. aureus, P. aeruginosa, and K. pneumonia (MICs = 25, 13, 6, and 21 μg/cm3, respectively). Hirsutide also has antifungal activity against C. albicans, M. audouinii, A. niger, and Ganoderma (MICs = 13, 6, 25, and 6 μg/cm3, respectively).

Palmitic acid-13C is intended for use as an internal standard for the quantification of palmitic acid by GC- or LC-MS. Palmitic acid-13C contains 13C at the C2 position and has been used in the study of free fatty acid incorporation into phospholipid fatty acids in soil microbes.1 Palmitic acid is a 16-carbon saturated fatty acid. It comprises approximately 25% of human total plasma lipids.2 It increases protein levels of COX-2 in RAW 264.7 cells when used at a concentration of 75 μM.3 Palmitic acid is involved in the acylation of proteins to anchor membrane-bound proteins to the lipid bilayer.3,4,5,6,7 |1. Dippold, M.A., and Kuzyakov, Y. Direct incorporation of fatty acids into microbial phospholipids in soils: Position-specific labeling tells the story. Geochim. Cosmochim. Acta 174(1), 211-221 (2016).|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 patients. Ann. Nutr. Metab. 39(1), 52-62 (1995).|3. Lee, J.Y., Sohn, K.H., Rhee, S.H., et al. Saturated fatty acids, but not unsaturated fatty acids, induced the expression of cyclooxygenase-2 mediated through toll-like receptor 4. J. Biol. Chem. 276(20), 16683-16689 (2001).|4. Dietzen, D.J., Hastings, W.R., and Lublin, D.M. Caveolin is palmitoylated on multiple cysteine residues. Palmitoylation is not necessary for localization of caveolin to caveolae. J. Biol. Chem. 270(12), 6838-6842 (1995).|5. Robinson, L.J., and Michel, T. Mutagenesis of palmitoylation sites in endothelial nitric oxide synthase identifies a novel motif for dual acylation and subcellular targeting. Proc. Nat. Acad. Sci. USA 92(25), 11776-11780 (1995).|6. Topinka, J.R., and Bredt, D.S. N-terminal palmitoylation of PSD-95 regulates association with cell membranes and interaction with K+ channel Kv1.4. Neuron 20(1), 125-134 (1998).|7. Miggin, S.M., Lawler, O.A., and Kinsella, B.T. Palmitoylation of the human prostacyclin receptor. Functional implications of palmitoylation and isoprenylation. J. Biol. Chem. 278(9), 6947-6958 (2003).

25-Desacetyl rifampicin is a major active metabolite of the rifamycin antibiotic rifampicin .125-Desacetyl rifampicin is active againstM. smegmatis(MIC99= 2.66 μM). 1.Kigondu, E.M., Njoroge, M., Singh, K., et al.Synthesis and synergistic antimycobacterial screening of chlorpromazine and its metabolitesMed. Chem. Commun.5502-506(2014)

Inostamycin A is a bacterial metabolite that has been found inStreptomycesand has anticancer activity.1It is an inhibitor of CDP-diacylglycerol:inositol 3-phosphatidyltransferase (IC50= 0.02 μg/ml in A431 cell membranes) and is selective for CDP-diacylglycerol:inositol 3-phosphatidyltransferase over phospholipase C (PLC) and phosphatidylinositol kinase at 10 μg/ml.2Inostamycin A decreases viability of YCU-T892, KCC-TC873, KB, HSC-4, and YCU-T891 oral squamous cell carcinoma (OSCC) cells in a concentration-dependent manner.3It induces cell cycle arrest in the G1phase in HSC-4 cells when used at a concentration of 250 ng/ml and induces apoptosis in Ms-1 small cell lung cancer cells at 300 ng/ml.3,4Inostamycin A also reduces levels of matrix metalloproteinase-2 (MMP-2) and MMP-9 and inhibits EGF-induced migration of HSC-4 cells.5 1.Imoto, M., Umezawa, K., Takahashi, Y., et al.Isolation and structure determination of inostamycin, a novel inhibitor of phosphatidylinositol turnoverJ. Nat. Prod.53(4)825-829(1990) 2.Imoto, M., Taniguchi, Y., and Umezawa, K.Inhibition of CDP-DG: inositol transferase by inostamycinJ. Biochem.112(2)299-302(1992) 3.Baba, Y., Tsukuda, M., Mochimatsu, I., et al.Cytostatic effect of inostamycin, an inhibitor of cytidine 5'-diphosphate 1,2-diacyl-sn-glycerol (CDP-DG): inositol transferase, on oral squamous cell carcinoma cell linesCell Biol. Int.25(7)613-620(2001) 4.Imoto, M., Tanabe, K., Simizu, S., et al.Inhibition of cyclin D1 expression and induction of apoptosis by inostamycin in small cell lung carcinoma cellsJpn. J. Cancer Res.89(3)315-322(1998) 5.Baba, Y., Tsukuda, M., Mochimatsu, I., et al.Inostamycin, an inhibitor of cytidine 5'-diphosphate 1,2-diacyl-sn-glycerol (CDP-DG): Inositol transferase, suppresses invasion ability by reducing productions of matrix metalloproteinase-2 and -9 and cell motility in HSC-4 tongue carcinoma cell lineClin. Exp. Metastasis18(3)273-279(2000)

Betamethasone 21-phosphate is a synthetic glucocorticoid.1It prevents increases in macrophage and eosinophil numbers in bronchoalveolar lavage fluid (BALF) and decreases in blood leukocyte numbers in a guinea pig model of parainfluenza-3 viral infection when administered at a dose of 8 mg/kg but does not prevent airway hyperresponsiveness after infection.2Betamethasone 21-phosphate inhibits cell infiltration into the aqueous humor in a rat model of endotoxin-induced uveitis when administered topically or subcutaneously at doses of 0.01-1% or 1 mg/kg, respectively.3It increases maximal lung pressure volume curves in fetal sheep when administered to pregnant ewes at 0.75 gestation at doses of 80 and 170 μg/kg.1Betamethasone 21-phosphate increases body weight, impairs learning and memory, increases anxiolytic behavior, and reduces hippocampal neurogenesis in CD-1 mice but reduces body weight and increases neurogenesis with no effect on anxiety in high-anxiety DBA/2 mice when administered at a dose of approximately 25 mg/kg per day in the drinking water for seven weeks.4Formulations containing betamethasone 12-phosphate and betamethasone acetate have been used in the treatment of severe allergic conditions and a variety of immune-related conditions. 1.Loehle, M., Schwab, M., Kadner, S., et al.Dose-response effects of betamethasone on maturation of the fetal sheep lungAm. J. Obstet. Gynecol.202(2)186.e181-186.e187(2010) 2.Leusink-Muis, A., Ten Broeke, R., Folkerts, G., et al.Betamethasone prevents virus-induced airway inflammation but not airway hyperresponsiveness in guinea pigsClin. Exp. Allergy29(Suppl. 2)82-85(1999) 3.Tsuji, F., Sawa, K., Kato, M., et al.The effects of betamethasone derivatives on endotoxin-induced uveitis in ratExp. Eye Res.64(1)31-36(1997) 4.Aiello, R., Crupi, R., Leo, A., et al.Long-term betamethasone 21-phosphate disodium treatment has distinct effects in CD1 and DBA/2 mice on animal behavior accompanied by opposite effects on neurogenesisBehav. Brain Res.278155-166(2015)

4-CPPC is an inhibitor of macrophage migration inhibitory factor-2 (MIF-2; IC50= 27 μM).1It is selective for MIF-2 over MIF-1 (IC50= 450 μM). It inhibits MIF-2, but not MIF-1, binding to CD74in vitrowhen used at a concentration of 10 μM. 4-CPPC (5, 10, and 25 μM) inhibits MIF-2-induced ERK1/2 phosphorylation in primary human skin fibroblasts. 1.Tilstam, P.V., Pantouris, G., Corman, M., et al.A selective small-molecule inhibitor of macrophage migration inhibitory factor-2 (MIF-2), a MIF cytokine superfamily member, inhibits MIF-2 biological activityJ. Biol. Chem.294(49)18522-18531(2019)

2-(1-(Thiophen-2-yl)ethylidene)hydrazinecarbothioamide is an antimicrobial agent.1It is active against the Gram-negative bacteriaE. coli,P. aeruginosa, andS. marcescens(MICs = 64, 100, and 70 μg/ml, respectively), the Gram-positive bacteriaS. aureus,M. luteus, andB. cereus(MICs = 130, 100, and 50 μg/ml, respectively), and the fungiC. albicans,G. candidum,T. rubrum,F. oxysporum,A. flavus, andS. brevicaulis(MICs = 69-120 μg/ml). 2-(1-(Thiophen-2-yl)ethylidene)hydrazinecarbothioamide is also a precursor in the synthesis of other antimicrobial agents, as well as compounds with anticancer activity.1,2 1.Youssef, M.S.K., and Abeed, A.A.O.Synthesis and antimicrobial activity of some novel 2-thienyl substituted heterocyclesHeterocycl. Commun.20(1)25-31(2014) 2.Gomha, S.M., Edrees, M.M., and Altalbawy, F.M.A.Synthesis and characterization of some new bis-pyrazolyl-thiazoles incorporating the thiophene moiety as potent anti-tumor agentsInt. J. Mol. Sci.17(9)1499(2016)

Antitubercular agent-25 (Compound 28) is an anti-tubercular agent with an extracellular IC50 of 0.42 μM and an intracellular IC50 of 0.20 μM against M. tuberculosis H37Rv, and it demonstrates good metabolic stability.

7-oxo Staurosporine is an antibiotic originally isolated from S. platensis with diverse biological activites. It inhibits PKC, PKA, phosphorylase kinase, EGFR, and c-Src in vitro (IC50s = 9, 26, 5, 200, and 800 nM, respectively). 7-oxo Staurosporine induces cell cycle arrest in the G2/M phase in human leukemia K562 cells with a minimal effective dose (MED) of 30 ng/ml. It is cytotoxic to P388 mouse leukemia cells that are resistant and susceptible to doxorubicin . 7-oxo Staurosporine inhibits growth of the mycelial, but not yeast form of C. albicans, C. krusei, C. tropicalis, and C. lusitaniae (MICs = 3.1-25 μg/ml). It increases sphingomyelin synthesis in CHO-K1 cells when used at a concentration of 50 nM.

Pericosine A is a fungal metabolite that has been found inP. byssoidesand has anticancer activity.1It inhibits the growth of a variety of cancer cells, including breast, colon, lung, ovary, stomach, and prostate cell lines (GI50s = 0.05-24.55 μM) and increases survival in a P388 mouse xenograft model when administered at a dose of 25 mg/kg. Pericosine A inhibits EGFR by 40 to 70% when used at a concentration of 100 μg/ml. It also reacts with organosulfur compounds in skunk spray to form stable thioethers as odorless products.2 1.Yamada, T., Iritani, M., Ohishi, H., et al.Pericosines, antitumour metabolites from the sea hare-derived fungus Periconia byssoides. Structures and biological activitiesOrg. Biomol. Chem.5(24)3979-3986(2007) 2.Du, L., Munteanu, C., King, J.B., et al.An electrophilic natural product provides a safe and robust odor neutralization approach to counteract malodorous organosulfur metabolites encountered in skunk sprayJ. Nat. Prod.82(7)1989-1999(2019)

(±)10-HDHA is an autoxidation product of docosahexaenoic acid (DHA) in vitro.[1][2] It is also produced from incubations of DHA in rat liver, brain, and intestinal microsomes.[3][4][5] (±)10-HDHA is a potential marker of oxidative stress in brain and retina where DHA is an abundant polyunsaturated fatty acid. Reference：[1]. VanRollins, M., and Murphy, R.C. Autooxidation of docosahexaenoic acid: Analysis of ten isomers of hydroxydocosahexaenoate. J. Lipid Res. 25(5), 507-517 (1984).[2]. Reynaud, D., Thickitt, C.P., and Pace-Asciak, C.R. Facile preparation and structural determination of monohydroxy derivatives of docosahexaenoic acid (HDoHE) by α-tocopherol-directed autoxidation. Anal. Biochem. 214(1), 165-170 (1993).[3]. VanRollins, M., Baker, R.C., Sprecher, H., et al. Oxidation of docosahexaenoic acid by rat liver microsomes. J. Biol. Chem. 259(9), 5776-5783 (1984).[4]. Yamane, M., Abe, A., and Yamane, S. High-performance liquid chromatography-thermospray mass spectrometry of epoxy polyunsaturated fatty acids and epoxyhydroxy polyunsaturated fatty acids from an incubation mixture of rat tissue homogenate. J. Chromatogr. 652(2), 123-136 (1994).[5]. Kim, H.Y., Karanian, J.W., Shingu, T., et al. Sterochemical analysis of hydroxylated docosahexaenoates produced by human platelets and rat brain homogenate. Prostaglandins 40(5), 473-490 (1990).

Azurin (50-77) is a peptide fragment derived from the copper-containing bacterial protein azurin, present in P. aeruginosa. It exhibits properties that regulate the cell cycle, inhibit cancer proliferation, and manage angiogenesis, proving its potential as an anticancer agent. Specifically, this compound acts as a VEGFR2 inhibitor with an IC20 of approximately 10.7 µM. At a concentration of 20 µM, it effectively induces cell cycle arrest at the G2/M phase in MCF-7 breast cancer cells, while a higher concentration of 50 µM significantly reduces the proliferation of both MCF-7 and ZR-75-1 breast cancer cell lines. Furthermore, Azurin (50-77) impedes VEGF-A-induced capillary tube formation with an IC50 of 12 µM, and alters the cellular and extracellular levels of critical signaling and structural proteins such as F-actin, focal adhesion kinase (FAK), paxillin, and platelet endothelial cell adhesion molecule-1 (PECAM-1) in human umbilical vein endothelial cells (HUVECs) at a concentration of 25 µM. Demonstrating its efficacy in vivo, Azurin (50-77) administered at 10 mg/kg per day notably reduces tumor volume in an MCF-7 mouse xenograft model, highlighting its therapeutic potential.

m-PEG25-acid is a PEG-based linker for PROTACs that joins two essential ligands, crucial for forming PROTAC molecules, enabling selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

1-Isothiocyanato-6-(methylsulfenyl)-hexane, identified in wasabi (W. japonica), exhibits multifaceted biological activities. This isothiocyanate compound demonstrates antibacterial properties by inhibiting B. subtilis growth in an agar diffusion assay at 25 µmol/disc, and antifungal effectiveness against T. mentagrophytes with a minimum inhibitory concentration (MIC) of 25 µg/ml. Additionally, it acts as a repellent in the blue mussel (M. edulis) assay and shows antifouling capabilities on polyvinyl chloride (PVC) plates at a concentration of 50 µmol/cm^2, underscoring its potential in biotechnological applications.

PGA2 is a naturally occurring prostaglandin in gorgonian corals where it may function in self defense. It is generally not present in mammals. PGA2 has low biological potency in most bioassays, but it does show some antiviral/antitumor activity.[1] At a 25 uM concentration, PGA2 blocks the cell cycle progression of NIH 3T3 cells at the G1 and G2/M phase .[2] It has also been shown to act as a vasodilator with natriuretic properties.[3]

TAS-103 is a dual inhibitor of DNA topoisomerase I II, utilized in cancer research.

3-epi-25-hydroxy Vitamin D3 is the C-3 epimer of 25-hydroxy vitamin D3. Dietary administration of 3-epi-25-hydroxy vitamin D3 (0.5 and 1 IU g) decreases levels of serum parathyroid hormone (PTH) in male, but not female, weanling rats.

β-Rubromycin is a bacterial metabolite originally isolated from Streptomyces that has diverse biological activities.1 It inhibits the growth of HMO2, KATO-III, and MCF-7 cells with GI50 values of 0.5, 0.84, and <0.1 μM, respectively. β-rubromycin inhibits HIV-1 reverse transcriptase activity by 39.7% when used at a concentration of 10 μM. It also has antibacterial activity against Gram-positive bacteria. The structure of β-rubromycin was originally described as containing an ortho-quinone group, but it was revised to a para-quinone group in 2000 using organic and biosynthetic methods, as well as spectroscopic analysis.1,2,3References1. Ueno, T., Takahashi, H., Oda, M., et al. Inhibition of human telomerase by rubromycins: Implication of spiroketal system of the compounds as an active moiety. Biochemistry 39(20), 5995-6002 (2000).2. Puder, C., Loya, S., Hizi, A., et al. Structural and biosynthetic investigations of the rubromycins. Eur. J. Org. Chem. 2000(5), 729-735 (2000).3. Goldman, M.E., Salituro, G.S., Bowen, J.A., et al. Inhibition of human immunodeficiency virus-1 reverse transcriptase activity by rubromycins: Competitive interaction at the template.primer site. Mol. Pharmacol. 38(1), 20-25 (1990). β-Rubromycin is a bacterial metabolite originally isolated from Streptomyces that has diverse biological activities.1 It inhibits the growth of HMO2, KATO-III, and MCF-7 cells with GI50 values of 0.5, 0.84, and <0.1 μM, respectively. β-rubromycin inhibits HIV-1 reverse transcriptase activity by 39.7% when used at a concentration of 10 μM. It also has antibacterial activity against Gram-positive bacteria. The structure of β-rubromycin was originally described as containing an ortho-quinone group, but it was revised to a para-quinone group in 2000 using organic and biosynthetic methods, as well as spectroscopic analysis.1,2,3 References1. Ueno, T., Takahashi, H., Oda, M., et al. Inhibition of human telomerase by rubromycins: Implication of spiroketal system of the compounds as an active moiety. Biochemistry 39(20), 5995-6002 (2000).2. Puder, C., Loya, S., Hizi, A., et al. Structural and biosynthetic investigations of the rubromycins. Eur. J. Org. Chem. 2000(5), 729-735 (2000).3. Goldman, M.E., Salituro, G.S., Bowen, J.A., et al. Inhibition of human immunodeficiency virus-1 reverse transcriptase activity by rubromycins: Competitive interaction at the template.primer site. Mol. Pharmacol. 38(1), 20-25 (1990).

Beauvericin A is a cyclodepsipeptide and derivative of beauvericin originally isolated fromB. bassianathat has diverse biological activities.1,2,3It is active againstM. tuberculosis(MIC = 25 μg/ml) andP. falciparum(IC50= 12 μg/ml).2Beauvericin A is toxic to brine shrimp (LD100= 32 μg/ml).3 1.Gupta, S., Montillor, C., and Hwang, Y.-S.Isolation of Novel Beauvericin Analogues from the Fungus Beauveria bassianaJ. Nat. Prod.58(5)733-738(1995) 2.Nilanonta, C., Isaka, M., Kittakoop, P., et al.Antimycobacterial and antiplasmodial cyclodepsipeptides from the insect pathogenic fungus Paecilomyces tenuipes BCC 1614Planta Med.66(8)756-758(2000) 3.Shi, S., Li, Y., Ming, Y., et al.Biological activity and chemical composition of the endophytic fungus Fusarium sp. TP-G1 obtained from the root of Dendrobium officinale Kimura et MigoRec. Nat. Prod.12(6)549-556(2018)

Gilvocarcin M is an antibiotic originally isolated from S. gilvotanareus. It is active against S. aureus when used at a concentration of 32 μg/ml. Gilvocarcin M inhibits growth of KB cells (IC50 = 0.52 μg/ml) but has no effect on survival in a P388 mouse model of leukemia when used at doses ranging from 25 to 400 mg/kg. Gilvocarcin M intercalates into bacteriophage PM2 DNA. It is toxic to rats with an intravenous LD50 value of 450 mg/kg.

Terrecyclic acid is a sesquiterpene originally isolated from A. terreus with antibiotic and anticancer activity. It is active against S. aureus, B. subtilis, and M. roseus (MICs = 25, 50, and 25 μg ml, respectively). Terrecyclic acid induces a heat shock response, increases levels of reactive oxygen species (ROS), and inhibits NF-κB activity and cell growth in 3T3-Y9-B12 cells.

α/β-Hydrolase-IN-1 demonstrates exceptional potency, with MICs of 50 μM (25 μg/mL) against M. smegmatis and 16 μM (8.4 μg/mL) against M. tuberculosis H37Ra, establishing it as a superior compound in this class.

m-PEG25-NHS ester is a PEG-based linker for PROTACs that connects two essential ligands for the formation of PROTAC molecules, enabling selective protein degradation via the ubiquitin-proteasome system within cells.

Aurein 2.6, an antibiotic antimicrobial peptide, exhibits activity against various Gram-positive bacteria with minimum inhibitory concentrations (MIC) of 25, 25, 30, 25, and 30 μM for M. luteus, S. aureus, S. epidermis, S. mutans, and B. subtilis, respectively [1][2].

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)

m-PEG25-Hydrazide is a PEG-based linker for PROTACs that connects two essential ligands, facilitating the formation of PROTAC molecules and enabling selective protein degradation by utilizing the ubiquitin-proteasome system within cells.

Thujopsene, a sesquiterpene found in T. dolabrata, exhibits a wide range of biological activities. It inhibits Na+/K+-ATPase and cytochrome P450 (CYP) isoform CYP2B6 with IC50 values of 25.9 µg/ml and Ki of 0.8 µM, respectively. Additionally, thujopsene demonstrates antimicrobial efficacy against both Gram-positive and Gram-negative bacteria, such as S. aureus, M. luteus, and S. typhimurium, with MICs ranging from 25-50 µg/ml. It also suppresses antigen-induced β-hexosaminidase release in IgE-sensitized RBL-2H3 mast cells (IC50= 25.1 µM) and shows cytotoxicity against A549 non-small cell lung cancer cells with an LC50 of 35.27 µg/ml. Furthermore, thujopsene causes mortality in mites D. farinae and T. putrescentiae, with LC50s of 9.82 and 10.92 µg/cm2, respectively.

Mn(III)TMPyP is a manganese-porphyrin which acts as a superoxide dismutase (SOD) mimetic and peroxynitrite decomposition catalyst. SOD mimetics described to date are unstable and are capable of catalyzing undesired side-reactions in addition to the dismutation of the superoxide radical (O2-). Mn(III)TMPyP is an SOD mimetic with increased stability to pH and hydrogen peroxide. The rate constant for superoxide dismutation and peroxynitrite decomposition are 3.9 x 107 M-1s-1 and ~2 x 106 M-1s-1, respectively. Mn(III)TMPyP protected and enhanced the growth of SOD E. coli with a doubling time of 60 minutes (as compared to 240 minutes of the control) at 25 µM.

Carbazomycin D is a bacterial metabolite that has been found inStreptomycesand has diverse biological activities.1,2It is active against the fungiT. asteroidesandT. mentagrophytes(MIC = 100 μg/ml for both) and the bacteriumM. tuberculosis(IC50= 25 μg/ml). Carbazomycin D is cytotoxic to MCF-7, KB, NCI H187, and Vero cells (IC50s = 21.3, 33.2, 12.9, and 34.3 μg/ml, respectively).2 1.Naid, T., Kitahara, T., Kaneda, M., et al.Carbazomycins C, D, E and F, minor components of the carbazomycin complexJ. Antibiot. (Tokyo)40(2)157-164(1987) 2.Intaraudom, C., Rachtawee, P., Suvannakad, R., et al.Antimalarial and antituberculosis substances from Streptomyces sp. BCC26924Tetrahedron67(39)7593-7597(2011)

HT-2 toxin-13C22is intended for use as an internal standard for the quantification of HT-2 toxin by GC- or LC-MS. HT-2 toxin is a type A trichothecene mycotoxin and an active, deacetylated metabolite of the trichothecene mycotoxin T-2 toxin .1,2Like T-2 toxin, HT-2 toxin inhibits protein synthesis and cell proliferation in plants.2HT-2 toxin also reduces viability of HepG2, A549, HEp-2, Caco-2, A-204, U937, Jurkat, and RPMI-8226 cancer cells with IC50values ranging from 3.1 to 23 ng/ml and human umbilical vein endothelial cells with an IC50value of 56.4 ng/ml.1It induces oxidative stress, DNA damage, and autophagy in, as well as halts the development of, cultured mouse embryos when used at a concentration of 10 nM.3HT-2 toxin has been found in cereal grains and food products.4,5 1.Nielsen, C., Casteel, M., Didier, A., et al.Trichothecene-induced cytotoxicity on human cell linesMycotoxin Res.25(2)77-84(2009) 2.Nathanail, A.V., Varga, E., Meng-Reiterer, J., et al.Metabolism of the fusarium mycotoxins T-2 toxin and HT-2 toxin in wheatJ. Agric. Food Chem.63(35)7862-7872(2015) 3.Zhang, L., Li, L., Xu, J., et al.HT-2 toxin exposure induces mitochondria dysfunction and DNA damage during mouse early embryo developmentReprod. Toxicol.85104-109(2019) 4.Langseth, W., and Rundberget, T.The occurrence of HT-2 toxin and other trichothecenes in Norwegian cerealsMycopathologia147(3)157-165(1999) 5.Al-Taher, F., Cappozzo, J., Zweigenbaum, J., et al.Detection and quantitation of mycotoxins in infant cereals in the U.S. market by LC-MS/MS using a stable isotope dilution assayFood Control72(Part A)27-35(2017)

para-amino-Blebbistatin is a more water-soluble form of (S)-4'-nitro-blebbistatin , which is a more stable and less phototoxic form of (-)-blebbistatin .1,2,3 (-)-Blebbistatin is a selective cell-permeable inhibitor of non-muscle myosin II ATPases that rapidly and reversibly inhibits Mg-ATPase activity and in vitro motility of non-muscle myosin IIA and IIB for several species (IC50s = 0.5-5 μM), while poorly inhibiting smooth muscle myosin (IC50 = 80 μM).2,3,4 Through these effects, it blocks apoptosis-related bleb formation, directed cell migration, and cytokinesis in vertebrate cells. However, prolonged exposure to blue light (450-490 nm) results in degradation of blebbistatin to an inactive product via cytotoxic intermediates, which may be problematic for its use in fluorescent live cell imaging applications.5,6 The addition of a 4'-amino group increases its water solubility, decreases the inherent fluorescence, stabilizes the molecule to circumvent its degradation by prolonged blue light exposure, and decreases its phototoxicity while retaining the in vitro and in vivo activity of blebbistatin.7 para-amino-Blebbistatin has the same stereochemistry as the active (-)-blebbistatin enantiomer. |1. Várkuti, B.H., Képiró, M., Horváth, I.á., et al. A highly soluble, non-phototoxic, non-fluorescent blebbistatin derivative. Sci. Rep. 6:26141, (2016).|2. Straight, A.F., Cheung, A., Limouze, J., et al. Dissecting temporal and spatial control of cytokinesis with a myosin II inhibitor. Science 299(5613), 1743-1747 (2003).|3. Kovács, M., Tóth, J., Hetényi, C., et al. Mechanism of blebbistatin inhibition of myosin II. J. Biol. Chem. 279(34), 35557-35563 (2004).|4. Limouze, J., Straight, A.F., Mitchison, T., et al. Specificity of blebbistatin, an inhibitor of myosin II. J. Muscle Res. Cell Motil. 25(4-5), 337-341 (2004).|5. Kolega, J. Phototoxicity and photoinactivation of blebbistatin in UV and visible light. Biochem. Biophys. Res. Commun. 320(3), 1020-1025 (2004).|6. Sakamoto, T., Limouze, J., Combs, C.A., et al. Blebbistatin, a myosin II inhibitor, is photoinactivated by blue light. Biochemistry 44(2), 584-588 (2005).|7. Verhasselt, S., Roman, B.I., Bracke, M.E., et al. Improved synthesis and comparative analysis of the tool properties of new and existing D-ring modified (S)-blebbistatin analogs. Eur. J. Med. Chem. 136, 85-103 (2017).