DG-041 is a selective EP3 receptor antagonist for antiplatelet research
**Background**
Prostaglandin E2 (PGE2) is a key lipid mediator that exerts various physiological effects through its interaction with four G protein-coupled receptors: EP1, EP2, EP3, and EP4. Among these, the EP3 receptor plays a critical role in modulating platelet aggregation and various neurological functions. Because PGE2 facilitation of platelet aggregation is a significant factor in thrombotic events, the development of selective EP3 receptor antagonists has become a focal point for creating novel antiplatelet agents that do not prolong bleeding time. Furthermore, the ability of such compounds to cross the blood-brain barrier opens possibilities for treating central nervous system disorders. In this context, we will introduce a potent and selective EP3 receptor antagonist – DG-041.
**Definition**
DG-041 is a high-affinity and selective EP3 receptor antagonist with IC50 values of 4.6 nM in binding assays and 8.1 nM in FLIPR assays.
**In Vitro and In Vivo Studies**
According to the DG-041 description, this compound is a heterocyclic 1,7-disubstituted indole sulfonamide. In terms of DG-041 biological activity, in vitro studies demonstrated that it is highly selective for the EP3 receptor, exhibiting significantly lower potency against other receptors, including DP1 (IC50 = 131 nM), EP1 (IC50 = 486 nM), and TP receptors (IC50 = 742 nM). In cellular assays using human platelet-rich plasma, DG-041 exhibited antiplatelet activity by inhibiting collagen and sulprostone-induced platelet aggregation with an IC50 of 218 nM.
Regarding DG-041 in vivo performance, studies conducted in male SpragueDawley rats showed that the compound is well-absorbed. When administered intravenously at 1.78 mg/kg, it reached a Cmax of 9.46 μM with a half-life (t1/2) of 2.7 hours. When administered orally at 9.62 mg/kg, the Cmax was 2.74 μM with a t1/2 of 4.06 hours. The clearance (CL) for intravenous administration was recorded at 1250 mL/h/kg. Additionally, it has been confirmed that DG-041 crosses the blood-brain barrier. In conclusion, DG-041 is a potent, selective EP3 receptor antagonist that effectively inhibits PGE2-mediated platelet aggregation.
Keywords
DG-041, 861238-35-9, DG041, DG 041, Prostaglandin Receptor, blood-brain, barrier, Myocardial, infarction, stroke, atherosclerotic, plaque, atherothrombosis, Inhibitor, inhibitor
References
[1] Singh J, et al. Antagonists of the EP3 receptor for prostaglandin E2 are novel antiplatelet agents that do not prolong bleeding. ACS Chem Biol. 2009 Feb 20;4(2):115-26.
[2] Hategan G, et al. Heterocyclic 1,7-disubstituted indole sulfonamides are potent and selective human EP3 receptorantagonists. Bioorg Med Chem Lett. 2009 Dec 1;19(23):6797-800.
**Background**
Cardiovascular diseases (CVDs) remain a leading cause of morbidity and mortality worldwide. Among the various enzymatic targets involved in the progression of these conditions, chymase—a serine protease primarily expressed in mast cells—plays a critical role. Chymase is involved in the conversion of angiotensin I to angiotensin II, the degradation of extracellular matrix proteins, and the promotion of inflammation and fibrosis in the heart and blood vessels. Due to its involvement in cardiac remodeling and hypertension, the development of selective chymase inhibitors has become a significant focus for therapeutic intervention in cardiovascular research. In this context, we will introduce a selective chymase inhibitor – 6-Chlorooxindole.
**Definition**
6-Chlorooxindole is a selective chymase inhibitor with an IC50 value of 470 μM. According to the 6-Chlorooxindole description, this compound is utilized as a chemical tool to modulate chymase activity in biological systems.
**Biological Activity**
The 6-Chlorooxindole biological activity is characterized by its high selectivity for its target. Specifically, 6-Chlorooxindole shows >100-fold selectivity for chymase over cathepsin G, which is essential for minimizing off-target effects in experimental models. Based on the 6-Chlorooxindole technical information, the compound possesses a molecular weight of 167.59 and a chemical formula of C8H6ClNO. Research utilizing this inhibitor has focused on the discovery of potent and selective chymase inhibitors through fragment linking strategies, providing a foundation for studying the inhibition of protease-driven cardiovascular pathology. In conclusion, 6-Chlorooxindole is a selective chymase inhibitor that serves as a valuable tool for the study of cardiovascular disease.
Keywords
6-Chlorooxindole, 56341-37-8, Proteasome, chymase inhibitor, cardiovascular disease, Inhibitor, inhibitor, inhibit
References
**Background**
Plant cell walls are complex structures that provide mechanical support and protection to flowering plants. Among the various components of the secondary plant cell wall, hemicelluloses play a critical role in maintaining structural integrity by cross-linking cellulose microfibrils. Xylan is recognized as the primary hemicellulose component in the secondary cell walls of flowering plants, particularly within the tracheary elements and fibers. Understanding the molecular flexibility and interaction of these polysaccharides with cellulose surfaces is essential for advancements in plant biology and bioenergy research. In this context, we will introduce a key plant polysaccharide – Xylan.
**Definition**
Xylan is a polysaccharide composed predominantly of $\beta$-D-xylose units linked in a manner similar to cellulose. According to the Xylan description, it serves as a major structural component in the secondary walls of tracheary elements and fibers, as well as the primary walls of parenchyma cells in grasses.
**In Vitro Studies**
Regarding Xylan in vitro activity, this polysaccharide consists of a linear chain of $\beta$-1,4-linked xylosyl residues. These chains are frequently decorated with 2-O-linked glucuronic acid (GlcA) or methylated glucuronic acid (MeGlcA), which modulate its biological properties. Research indicates that regular motifs within the xylan structure are crucial for modulating molecular flexibility and its specific interactions with cellulose surfaces. Furthermore, the regiospecific acetylation of xylan is mediated by a specific group of DUF231-containing O-acetyltransferases, highlighting the complex enzymatic regulation of its structure. For researchers seeking detailed Xylan technical information, these structural modifications are key to understanding how the polysaccharide functions within the plant matrix. In conclusion, Xylan is a fundamental plant polysaccharide essential for the structural organization of secondary cell walls.
Keywords
Xylan, 9014-63-5, Endogenous Metabolite, hemicellulose, secondary, plant, cell, walls, cellulose, Inhibitor, inhibitor, inhibit
References
[1] Martinez-Abad A, et al. Regular Motifs in Xylan Modulate Molecular Flexibility and Interactions with Cellulose Surfaces. Plant Physiol. 2017 Oct 25. pii: pp.01184.2017.
[2] Zhong R, et al. Regiospecific Acetylation of Xylan is Mediated by a Group of DUF231-Containing O-Acetyltransferases. Plant Cell Physiol. 2017;58(12):2126-2138.
**Background**
Cancer remains one of the most challenging diseases in modern medicine, requiring the development of potent chemotherapeutic agents to inhibit rapid tumor cell proliferation. Among the various strategies, the use of antimetabolites has proven effective in disrupting DNA and RNA synthesis. 5-Fluorouracil (5-FU) is a cornerstone of chemotherapy, but its clinical application is often limited by its short half-life and toxicity profile. To overcome these limitations, pro-drug strategies have been developed to provide a more sustained release of the active agent. In this context, we will introduce a chemotherapeutic 5-FU proagent used in the treatment of Tegafur Cancer – Tegafur.
**Definition**
Tegafur (also known as FT 207 or NSC 148958) is a 5-FU proagent that serves as a component of tegafur-uracil. According to the Tegafur description, it is designed to be bioactivated in the body to release 5-FU, thereby exerting cytotoxic effects on tumor cells.
**Mechanism of Action**
The Tegafur biological activity is characterized by its conversion into 5-FU by liver microsomal cytochrome P450 enzymes. Once converted, 5-FU is further metabolized intracellularly into two active metabolites: 5-fluoro-deoxyuridine-monophosphate (FdUMP) and 5-fluorouridine-triphosphate (FUTP). These metabolites act by inhibiting the enzyme thymidylate synthase and intercalating into RNA. This dual action results in decreased thymidine synthesis, reduced DNA synthesis, and disrupted RNA function, ultimately leading to tumor cell cytotoxicity.
**In Vitro Studies**
Tegafur in vitro studies have demonstrated significant antiproliferative and anticancer activity across various cell lines. In human cancer cells, Tegafur exhibited IC50 values of 172 μM in BXPC-3 cells and 201 μM in HT-29 cells after 72 hours of treatment. In the presence of succinate, the IC50 for BXPC-3 and HT-29 cells was reduced to 154 μM and 158 μM, respectively. Similarly, in mouse CT26 cells, the IC50 ranged from 90 μM (with succinate) to 136 μM. Other results include an IC50 of 1 μM in HUVEC cells after 48 hours and an IC50 of 384 μM in U-251 cells after 72 hours. Additionally, antiproliferative activity against human A549 and HCT-116 cells was measured with GI50 values of > 50 μM and > 10 μM, respectively, after 48 hours. In conclusion, Tegafur is a potent 5-FU proagent that effectively inhibits the growth of multiple cancer cell types.
Keywords
Tegafur, 17902-23-7, FT 207, NSC 148958, FT207, FT-207, NSC148958, NSC-148958, Nucleoside Antimetabolite/Analog, Inhibitor, inhibitor, inhibit
References
[1] Sotaro Sadahiro, Toshiyuki Suzuki, Akira Tanaka, et al. Association of right-sided tumors with high thymidine phosphorylase gene expression levels and the response to oral uracil and tegafur/leucovorin chemotherapy among patients with colorectal cancer. Cancer Chemotherapy and Pharmacology. 2012, 70 (2): 285-291.
[2] José L. Ariasa, et al. Engineering of an antitumor (core/shell) magnetic nanoformulation based on the chemotherapy agent ftorafur. Colloids and Surfaces A: Physicochemical and Engineering Aspects. 2011,384(1-3): 157-163.
[3] Gabriel N. Hortobagyi, William Heim, Laura Hutchins, et al. A phase 2 study of a fixed combination of uracil and ftorafur (UFT) and leucovorin given orally in a 3-times-daily regimen to treat patients with recurrent metastatic breast cancer. Cancer. 2010, 116(6): 1440-1445.
[4] K. Fujita, H. Nakayama, W. Ichikawa, et al. Pharmacokinetics of 5-Fluorouracil in Elderly Japanese Patients with Cancer Treated with S-1 (a Combination of Tegafur and Dihydropyrimidine Dehydrogenase Inhibitor 5-Chloro-2,4-dihydroxypyridine). Drug Metab Dispos. 2009 Jul;37(7):1375-7. doi: 10.1124/dmd.109.027052. Epub 2009 Apr 23.
[5] Tegafur-uracil
**Background**
Parkinson’s disease (PD) and restless legs syndrome (RLS) are debilitating neurological disorders characterized by motor dysfunction and sleep disturbances. A primary driver of these conditions is the deficiency of dopamine or the dysfunction of dopaminergic neurons in the brain. The dopamine D2-type receptor family, which includes D2, D3, and D4 receptors, plays a critical role in modulating motor control and reward pathways. Consequently, the development of selective agonists that can penetrate the blood-brain barrier (BBB) is essential for restoring dopaminergic signaling and improving patient outcomes. In this context, we will introduce a selective D2-type receptor agonist – Pramipexole dihydrochloride.
**Definition**
Pramipexole dihydrochloride is a blood-brain barrier penetrant dopamine D2-type receptor agonist. According to the Pramipexole dihydrochloride technical information, it exhibits high affinity for D2-type receptors, with Ki values of 3.9 nM for D2, 0.5 nM for D3, and 1.3 nM for D4 receptors.
**In Vitro and In Vivo Studies**
The Pramipexole dihydrochloride biological activity has been extensively evaluated across various models. In vitro studies demonstrate that the compound has low binding affinity for D1-type receptors, with an IC50 >50,000 nM. Furthermore, Pramipexole dihydrochloride in vitro (0.01-10 μM; 72 hours) has been shown to produce dose-dependent increases in soma size and dendritic arborization. It also attenuates levodopa-induced toxicity within mesencephalic cultures.
Regarding Pramipexole dihydrochloride In Vivo applications, research using male Wistar rats (250-300 g; 16-18 weeks old) demonstrated that administration of the compound (0.25-1 mg/kg; i.p.) significantly reduces infarction volume and improves neurological recovery following transient middle cerebral artery occlusion (tMCAO). These results suggest that the compound prevents ischemic cell death via mitochondrial pathways during ischemic stroke. In conclusion, Pramipexole dihydrochloride is a potent and selective D2-type receptor agonist suitable for research into Parkinson’s disease, restless legs syndrome, and ischemic stroke.
Keywords
Pramipexole dihydrochloride, 191217-81-9, Dopamine Receptor, Parkinson’s, disease, PD, restless, legs, syndrome, RLS, neurological, recovery, neuroprotection, tMCAO, transient, middle, cerebral, artery, occlusion, Inhibitor, inhibitor, inhibit
References
[1] Kvernmo, T., et al. A review of the receptor-binding and pharmacokinetic properties of dopamine agonists. Clin Ther, 2006. 28(8): p. 1065-78.
[2] Takashi Okura, et al. Blood-brain barrier transport of pramipexole, a dopamine D2 agonist. Life Sci. 2007 Apr 3;80(17):1564-71.
[3] Ginetta Collo, et al. Ropinirole and Pramipexole Promote Structural Plasticity in Human iPSC-Derived Dopaminergic Neurons via BDNF and mTOR Signaling. Neural Plast. 2018; 2018: 4196961.
[4] P M Carvey, et al. Attenuation of levodopa-induced toxicity in mesencephalic cultures by pramipexole. J Neural Transm (Vienna). 1997;104(2-3):209-28.
[5] Syed Suhail Andrabi, et al. Pramipexole prevents ischemic cell death via mitochondrial pathways in ischemic stroke. Dis Model Mech. 2019 Aug 1; 12(8): dmm033860.
**Background**
Artificial sweeteners are widely used in the food industry as low-calorie alternatives to sugar. However, emerging research suggests that long-term consumption of these compounds may have systemic effects beyond simple taste perception, potentially impacting metabolic homeostasis and cognitive function. In the context of oncology, certain sweeteners may influence the tumor microenvironment and the ability of cancer cells to evade the immune system. Specifically, the regulation of programmed death-ligand 1 (PD-L1) is a critical mechanism in cancer immune evasion, making the study of external chemical influences on this pathway highly significant. In this context, we will introduce a synthetic sweetener used in various biomedical studies – Acesulfame.
**Definition**
Acesulfame (Acesulfame potassium) is a synthetic sweetener with the molecular formula C4H4KNO4S. It is utilized in research to investigate neurometabolic functions, metabolic disorders, and the mechanisms of immune evasion in cancer.
**In Vitro and In Vivo Studies**
The Acesulfame description highlights its diverse biological impacts across different cell types and animal models. Regarding Acesulfame autophagy, in vitro studies demonstrated that Acesulfame (1 mM, 24 hours) activates the ERK1/2-mTORC1-ULK1 pathway to suppress the autophagic degradation of PD-L1 in RIL-175 (mouse hepatocellular carcinoma) and SK-Hep1 (human hepatocellular carcinoma) cells, thereby upregulating PD-L1 protein levels. Furthermore, this treatment increased granzyme B production in RIL-175 and SK-Hep1 cells when co-cultured with T cells. In neuroblastoma SH-SY5Y cells, Acesulfame (5-25 mM, 24 hours) inhibited mitochondrial metabolism, reduced the extracellular acidification rate (ECAR), and impaired ATP production and the phosphorylation of neuroprotective proteins.
Acesulfame in vivo data further reveal its systemic effects. In male and female CD-1 mice, oral administration of Acesulfame (37.5 mg/kg, p.o., once daily for 4 weeks) significantly altered the gut microbiome composition and increased body weight in males. Additionally, in C57BL/6J mice, administration via drinking water (12.5 mM) for 40 weeks led to a significant increase in fasting blood glucose and insulin levels, affecting neurometabolic functions without altering insulin sensitivity. In conclusion, Acesulfame is a synthetic sweetener that modulates metabolic, neurological, and immune-related pathways, serving as a valuable tool for studying Acesulfame Cancer and metabolic dysfunction.
Keywords
Acesulfame, 55589-62-3, PD-1/PD-L1, ERK, mTOR, Autophagy, PD-1/Programmed death-ligand 1, Extracellular signal regulated kinases, Mammalian target of Rapamycin, artificial, sweetener, neuro-metabolic, functions, cognitive, Inhibitor, inhibitor, inhibit
References
**Background**
Cyclic AMP-dependent protein kinase (PKA) is a critical enzyme in the signal transduction pathway that mediates the effects of various hormones and neurotransmitters. PKA consists of regulatory and catalytic subunits, where the catalytic subunit (cAK) is responsible for phosphorylating a wide array of target proteins, thereby regulating diverse cellular processes including metabolism, gene expression, and cell proliferation. Dysregulation of the PKA pathway is often associated with various pathological conditions, making the selective inhibition of cAK a significant target for biomedical research. In this context, we will introduce a potent cAK inhibitor – PKA-IN-1.
**Definition**
PKA-IN-1 is a potent and selective inhibitor of the cyclic AMP-dependent protein kinase (PKA) catalytic subunit (cAK) with an IC50 value of 0.03 μM.
**In Vitro Studies**
According to the PKA-IN-1 description, this compound acts as a competitive inhibitor with respect to ATP as a substrate. Regarding PKA-IN-1 biological activity, in vitro evaluations have demonstrated its high selectivity for cAK. Specifically, PKA-IN-1 In Vitro studies indicate that the compound is ineffective or serves as a very poor inhibitor against several other kinases, including wheat embryo Ca2+-dependent protein kinase (CDPK), rat brain Ca2+-dependent protein kinase C (PKC), chicken gizzard myosin light chain kinase (MLCK), and potato tuber cyclic nucleotide-binding phosphatase (Pase). This high degree of selectivity ensures that the observed biological effects are primarily attributed to the inhibition of the PKA catalytic subunit. For researchers requiring specific PKA-IN-1 technical information, such as the PKA-IN-1 Formula (C13H11N3O) or molecular weight (225.25), these details are essential for calculating precise experimental dosages. In conclusion, PKA-IN-1 is a highly selective and potent inhibitor of the PKA catalytic subunit.
Keywords
PKA-IN-1, 179985-52-5, PKA, Protein kinase A, cAK, Inhibitor, inhibitor, inhibit
References
**Background**
$\alpha/\beta$-hydrolase domain containing 6 (ABHD6) is a magnesium-dependent hydrolase that primarily acts as a monoacylglycerol lipase, targeting 2-arachidonoylglycerol (2-AG), one of the primary endocannabinoids in the mammalian nervous system. By regulating the levels of 2-AG, ABHD6 plays a critical role in modulating synaptic transmission and various physiological processes within the brain and peripheral tissues. Given its selective expression and enzymatic activity, ABHD6 has emerged as a significant therapeutic target for treating metabolic disorders and neurological diseases. Consequently, the development of potent and brain-penetrant inhibitors is essential for advancing research in these areas. In this context, we will introduce a selective ABHD6 inhibitor – KT185.
**Definition**
KT185 is an orally bioavailable and brain-penetrant selective ABHD6 inhibitor. According to the KT185 description, this compound exhibits high potency with an $\text{IC}_{50}$ value of 0.21 nM in Neuro2A cells.
**In Vitro and In Vivo Studies**
The chemical properties of this inhibitor are defined by the KT185 formula $\text{C}_{32}\text{H}_{33}\text{N}_5\text{O}_2$, with a molecular weight of 519.64. Regarding KT185 biological activity, in vitro studies have demonstrated its efficacy in various cellular environments. In HEK-293T cells expressing recombinant mouse ABHD6, KT185 exhibited an $\text{IC}_{50}$ of 13.6 nM. This activity was measured using 2-arachidonoylglycerol preincubated for 30 minutes, followed by substrate addition and analysis via LC-MS after an additional 30 minutes. Furthermore, the compound is characterized by its ability to penetrate the blood-brain barrier, making it a valuable tool for studying ABHD6 functions in the central nervous system. In vivo studies have confirmed that the piperidyl-1,2,3-triazole urea scaffold of KT185 provides the necessary potency and selectivity for active inhibition of ABHD6 in living models. In conclusion, KT185 is a potent, selective, and brain-penetrant inhibitor of ABHD6 suitable for pharmacological research.
Keywords
KT185, 1472640-86-0, KT 185, KT-185, MAGL, Monoacylglycerol lipase, Inhibitor, inhibitor, inhibit
References
**Background**
Chronic inflammation and oxidative stress are central drivers in the pathogenesis of various debilitating conditions, including neurodegenerative diseases, hepatotoxicity, and malignancy. In particular, the overactivation of signaling pathways such as NF-κB and the impairment of the Nrf2-mediated antioxidant response contribute to tissue damage and disease progression. For instance, in Parkinson’s disease, the loss of dopaminergic neurons is often exacerbated by inflammatory mediators, while in lung cancer, the epithelial-mesenchymal transition (EMT) promotes tumor invasiveness. Finding bioactive compounds that can modulate these complex pathways is critical for developing new therapeutic strategies. In this context, we will introduce a bioactive constituent of Rhododendron – Farrerol.
**Definition**
Farrerol is a flavonoid and polyphenol with the molecular formula C17H16O5 and a molecular weight of 300.31. It exhibits broad biological activities, including anti-oxidative, anti-inflammatory, anti-tumor, neuroprotective, and hepatoprotective effects.
**In Vitro and In Vivo Studies**
The Farrerol biological activity has been extensively studied across various models. In vitro, Farrerol observably reduces the production of inflammatory mediators, including IL-1β, IL-6, TNF-α, COX-2, and iNOS in LPS-induced RAW264.7 cells by suppressing the phosphorylation of AKT, ERK1/2, JNK1/2, and NF-κB p65. In microglia cell lines, it attenuates β-amyloid-induced oxidative stress and inflammation via the Nrf2/Keap1 pathway. Furthermore, Farrerol inhibits angiogenesis through the Akt/mTOR, Erk, and Jak2/Stat3 signaling pathways and overcomes the invasiveness of lung squamous cell carcinoma cells by regulating EMT inducers, demonstrating its potential in Farrerol cancer research. Additionally, it ameliorates acetaminophen-induced hepatotoxicity through the activation of Nrf2 and Farrerol autophagy.
In vivo studies further support these findings. Farrerol protects dopaminergic neurons in a rat model of Lipopolysaccharide-induced Parkinson’s disease by suppressing the activation of the AKT and NF-κB signaling pathways. In conclusion, Farrerol is a potent bioactive flavonoid that modulates multiple signaling pathways to exert protective effects against inflammation, oxidative stress, and tumor progression.
Keywords
Farrerol, 24211-30-1, (-)-Farrerol, Others, Inhibitor, inhibitor, inhibit
References
[1] Ran X, et al. Farrerol Ameliorates TNBS-Induced Colonic Inflammation by Inhibiting ERK1/2, JNK1/2, and NF-κB Signaling Pathway. Int J Mol Sci. 2018 Jul 13;19(7).
[2] Cui B, et al. Farrerol attenuates β-amyloid-induced oxidative stress and inflammation through Nrf2/Keap1 pathway in a microglia cell line. Biomed Pharmacother. 2019 Jan;109:112-119.
[3] Dai F, et al. Farrerol inhibited angiogenesis through Akt/mTOR, Erk and Jak2/Stat3 signal pathway. Phytomedicine. 2016 Jun 15;23(7):686-93.
[4] Li B, et al. Farrerol overcomes the invasiveness of lung squamous cell carcinoma cells by regulating the expression of inducers of epithelial mesenchymal transition. Microb Pathog. 2019 Jun;131:277.
[5] Li Y, et al. Farrerol protects dopaminergic neurons in a rat model of lipopolysaccharide-induced Parkinson’s disease by suppressing the activation of the AKT and NF-κB signaling pathways. Int Immunopharmacol. 2019 Oct;75:105739.
[6] Wang L, et al. Farrerol Ameliorates APAP-induced Hepatotoxicity via Activation of Nrf2 and Autophagy. Int J Biol Sci. 2019 Jan 29;15(4):788-799.
[7] Chen L, Yan T, Huang D, et al. Stereoselectivity of In Vivo Processes and Bioactivity of Farrerol Enantiomers. Molecules. 2025;30(9):2038.
**Background**
The endocannabinoid system plays a critical role in regulating various physiological processes, including mood, appetite, pain sensation, and memory. A central component of this system is the endocannabinoid 2-arachidonoylglycerol (2-AG), which acts as a potent agonist for cannabinoid receptors. The biosynthesis of 2-AG is primarily mediated by diacylglycerol lipase-β (DAGLβ), a principal biosynthetic enzyme. Given its role in the spatial and temporal regulation of endocannabinoid signaling in the brain, DAGLβ has become a significant target for understanding neurological functions and developing therapeutic interventions. In this context, we will introduce a selective inhibitor of this enzyme – DAGLβ-IN-1.
**Definition**
DAGLβ-IN-1 is a small molecule inhibitor of diacylglycerol lipase-β (DAGLβ) with the molecular formula C28H34F3N5O4.
**In Vitro Studies**
According to the DAGLβ-IN-1 description, this compound serves as a versatile intermediate for the design of DAGL-tailored activity-based probes. In terms of DAGLβ-IN-1 in vitro activity, the compound is utilized to study the inhibition of 2-AG biosynthesis. Research into the development and optimization of piperidyl-1,2,3-triazole ureas has demonstrated that such chemical probes can be selectively designed to target endocannabinoid biosynthesis. The DAGLβ-IN-1 technical information highlights its utility as a chemical tool to modulate the activity of DAGLβ, thereby allowing researchers to investigate the downstream effects of reduced 2-AG levels in various biological systems. In conclusion, DAGLβ-IN-1 is a selective DAGLβ inhibitor and a valuable intermediate for the creation of activity-based probes.
Keywords
DAGLβ-IN-1, 1402612-61-6, DAGL, Diacylglycerol lipase, DAG lipase, DGL, DAGLβ, diacylglycerol lipase-β, probes, Inhibitor, inhibitor, inhibit
References
[1] Ku-Lung Hsu, et al. Development and Optimization of Piperidyl-1,2,3-Triazole Ureas as Selective Chemical Probes of Endocannabinoid Biosynthesis. J Med Chem . 2013 Nov 14;56(21):8257-69.
[2] Tiziana Bisogno, et al. Cloning of the First sn1-DAG Lipases Points to the Spatial and Temporal Regulation of Endocannabinoid Signaling in the Brain. J Cell Biol. 2003 Nov 10;163(3):463-8.