Camoteskimab is a monoclonal antibody for autoinflammatory disease research
**Background**
Autoinflammatory diseases are characterized by inappropriate activation of the innate immune system, leading to systemic inflammation and tissue damage. Interleukin-18 (IL-18) is a potent pro-inflammatory cytokine that plays a critical role in the pathogenesis of various inflammatory conditions, including Adult-Onset Still’s Disease (AOSD) and atopic dermatitis. By triggering the production of interferon-gamma (IFN-γ) and other chemokines, IL-18 contributes to the chronic inflammatory cycle observed in these disorders. Consequently, targeting the IL-18 pathway has emerged as a promising therapeutic strategy to mitigate systemic inflammation and improve patient outcomes. In this context, we will introduce a fully human monoclonal antibody targeting IL-18 – Camoteskimab.
**Definition**
Camoteskimab is a fully human IgG1 kappa monoclonal antibody with high affinity for IL-18, exhibiting a binding affinity of 63 pM.
**In Vitro Studies**
According to the Camoteskimab description, this antibody is designed to neutralize the activity of IL-18 and inhibit the formation of the active IL-18/Ra/RB complex. In Camoteskimab In Vitro assays using PBMCs, the antibody potently neutralizes IL-18 activity with an IC50 in the sub-nanomolar range. Furthermore, the Camoteskimab biological activity has been validated through binding assays; immobilized human IL-18 protein binds to Camoteskimab with an EC50 of 201.8 ng/mL. Flow cytometric analysis using A431 cells further confirms its efficacy, where cells stained with the primary antibody at a 1/200 dilution showed significant binding compared to the Human IgG1 kappa isotype control. For researchers seeking detailed experimental parameters, the Camoteskimab protocol provides guidance on reconstitution using sterile PBS or saline. In conclusion, Camoteskimab is a high-affinity neutralizing antibody that serves as a powerful tool for studying the role of IL-18 in autoinflammatory diseases.
Keywords
Camoteskimab, 2492472-82-7, AVTX-007, CERC-007, MEDI 2338, AVTX007, AVTX 007, CERC007, CERC 007, MEDI2338, MEDI-2338, Interleukin Related, IL
References
[1] Bindoli S, et al. Adult-Onset Still’s Disease (AOSD): Advances in Understanding Pathophysiology, Genetics and Emerging Treatment Options. Drugs. 2024;84(3):257-274.
[2] Chen X, et al. Identification of cross-talk pathways and PANoptosis-related genes in periodontitis and Alzheimer’s disease by bioinformatics analysis and machine learning. Front Aging Neurosci. 2024 Aug 27;16:1430290.
[3] Richard Brown, et al. Anti-il-18 antibody therapy for treating atopic dermatitis. WO2024261470A1. 2025-12-20.
[4] Galozzi P, et al. Progress in Biological Therapies for Adult-Onset Still’s Disease. Biologics. 2022;16:21-34. Published 2022 Apr 21.
Chronic exposure to elevated manganese levels is increasingly recognized as a significant risk factor for neurocognitive and motor impairments, particularly in children. Despite this, the cellular mechanisms underlying manganese toxicity remain poorly understood, especially during the transition from physiological to toxic exposure levels. This study investigates Golgi Phosphoprotein 4 (GPP130) as a potential biomarker of manganese exposure in AF5 GABAergic neuronal cells, focusing on its specificity, sensitivity, and temporal dynamics. Our findings demonstrate that GPP130 degradation is highly specific to manganese among various divalent cations, including cobalt, copper, iron, nickel, and zinc, with no detectable degradation observed under any of these alternative exposures. Notably, GPP130 degradation occurs rapidly—within one hour of manganese exposure—and at remarkably low concentrations: as little as 0.54 µM Mn, which is approximately 200 times lower than previously reported thresholds. Crucially, this response occurs without measurable increases in intracellular manganese levels, indicating that GPP130 degradation is not a consequence of accumulated metal but rather an early signaling event in response to extracellular manganese flux.
Further analysis reveals that GPP130 degradation follows a biphasic pattern: initial rapid loss coincides with a transient spike in intracellular Mn, followed by a decline in both Mn levels and GPP130 protein over time, even under continued exposure. This suggests that GPP130 may play a regulatory role in manganese homeostasis, possibly facilitating efflux or redistribution. Recovery studies show that while GPP130 levels begin to rebound after cessation of exposure, recovery is slow and incomplete, underscoring the persistence of the cellular stress response.Neurogranin Proteinmedchemexpress In vivo validation in rats subchronically exposed to manganese via intraperitoneal injection (9.6 mg/kg/day, three times weekly for four weeks) confirms the relevance of these findings. Control animals exhibit GPP130 immunoreactivity in only 15–30% of striatal and cortical neurons, consistent with selective expression. After manganese exposure, there was a significant reduction in both the number of GPP130-positive cells and total protein levels across brain regions, confirming that GPP130 degradation is not limited to cell culture but reflects a real biological response in the intact nervous system.
These results establish GPP130 as a highly sensitive and specific cellular indicator of manganese exposure, capable of detecting perturbations at physiologically relevant levels.1,4-Dibromo-2,5-diiodobenzene site Its rapid, Mn-specific degradation provides insight into early molecular events in manganese neurotoxicity and supports a potential role in cellular manganese regulation.PMID:35094932 Given that GPP130 is involved in endosome-to-Golgi trafficking, its disruption may impair critical protein sorting pathways, contributing to functional deficits. Moreover, the observation that some neurons maintain GPP130 despite exposure suggests differential susceptibility across cell populations, potentially explaining regional vulnerability in manganese-induced neurotoxicity. These findings highlight GPP130 as a promising target for monitoring environmental manganese exposure and understanding early mechanisms of brain injury.MedChemExpress (MCE) offers a wide range of high-quality research chemicals and biochemicals (novel life-science reagents, reference compounds and natural compounds) for scientific use. We have professionally experienced and friendly staff to meet your needs. We are a competent and trustworthy partner for your research and scientific projects.Related websites: https://www.medchemexpress.com
**Background**
The G protein-coupled receptor 84 (GPR84) is a receptor primarily expressed in immune cells and is activated by medium-chain fatty acids. Activation of GPR84 plays a critical role in modulating inflammatory responses and the production of pro-inflammatory cytokines, such as interleukin-12 (IL-12). In the context of oncology, the modulation of the immune microenvironment is a key strategy for enhancing the efficacy of cancer therapies. Recent studies have highlighted the potential of GPR84 activation to trigger potent anti-tumor immune responses, making it an attractive target for treating various malignancies. Therefore, in this context, we will introduce a potent GPR84 activator – 3-Hydroxydodecanoic acid.
**Definition**
3-Hydroxydodecanoic acid is a medium-chain fatty acid and human endogenous metabolite that acts as an agonist of GPR84, exhibiting an EC50 value of 1.31 μM for the inhibition of forskolin-stimulated cAMP accumulation in CHO cells.
**In Vitro and In Vivo Studies**
According to the 3-Hydroxydodecanoic acid description, this compound serves as a powerful tool for studying immune-mediated tumor suppression. In vitro, 3-Hydroxydodecanoic acid (1-100 μM; 1 h) has been shown to induce lipid peroxidation in the rat cerebral cortex, resulting in increased TBA-RS levels. Furthermore, agonist activity was confirmed in CHO cell membranes co-expressing human GPR84 and beta-arrestin2, with an EC50 of 1.31 μM for cAMP inhibition and 3.25 μM for beta-arrestin 2 recruitment.
Regarding 3-Hydroxydodecanoic acid in vivo activity, the compound demonstrates significant anti-tumor effects in C57BL/6JRj mice bearing MC38 tumors. When administered via intraperitoneal injection (i.p.) on days 6, 9, and 12, it significantly reduced tumor growth. This effect was dependent on GPR84 receptor signaling and was characterized by increased IL-12 production and higher infiltration of CD8+ T cells within the tumors. Additionally, 3-Hydroxydodecanoic acid showed a strong synergistic anti-tumor effect when combined with 5-FU. These findings suggest that 3-Hydroxydodecanoic acid cancer research applications could extend to colon cancer, lung cancer, and melanoma. In conclusion, 3-Hydroxydodecanoic acid is a GPR84 agonist that promotes anti-tumor immunity via IL-12 production and T cell infiltration.
Keywords
3-Hydroxydodecanoic acid, 1883-13-2, Endogenous Metabolite, colon cancer, lung cancer, and melanoma, anticancer, mice., Inhibitor, inhibitor, inhibit
References
[1] Tonin AM, et al. Long-chain 3-hydroxy fatty acids accumulating in LCHAD and MTP deficiencies induce oxidative stress in rat brain. Neurochem Int. 2010 Jul;56(8):930-6.
[2] Katkeviciute E, et al. Bacteria-derived 3-hydroxydodecanoic acid induces a potent anti-tumor immune response via the GPR84 receptor. Cell Rep. 2025 Feb 26;44(3):115357.
**Background**
Obesity is a complex, chronic disease characterized by excessive adipose tissue accumulation, which significantly increases the risk of cardiovascular diseases, type 2 diabetes, and metabolic syndrome. The management of obesity often requires pharmacological interventions that target the central nervous system (CNS) to regulate appetite and energy expenditure. Monoamine neurotransmitters, including dopamine, norepinephrine, and serotonin, play critical roles in the modulation of food intake and satiety. Consequently, agents capable of modulating the synaptic levels of these neurotransmitters have become primary targets for the development of anti-obesity therapies. In this context, we will introduce a CNS-acting anti-obesity agent – Tesofensine.
**Definition**
Tesofensine (NS-2330) is a potent triple monoamine reuptake inhibitor that induces inhibition of the re-uptake process in the synaptic cleft for dopamine (IC50 = 6.5 nM), norepinephrine (IC50 = 1.7 nM), and serotonin (IC50 = 11 nM).
**In Vivo Studies**
According to the Tesofensine biological activity reported in literature, this compound demonstrates significant appetite-suppressing effects. In vivo studies using diet-induced obesity (DIO) rats showed that a single subcutaneous (s.c.) dose of Tesofensine (0.1-3 mg/kg) robustly and dose-dependently inhibits food intake over a 12-hour nocturnal observation period. The threshold dose for the inhibition of total food intake was found to be 1.0 mg/kg, with an estimated ED50 of 1.3 mg/kg. Furthermore, the Tesofensine protocol for chronic treatment involved daily subcutaneous administration of a moderate dose (2.0 mg/kg) over 16 days. This regimen triggered a significant reduction in body weight starting after 4 days of administration relative to vehicle-treated controls. Over the entire treatment period, the average relative decrease in body weight of treated DIO rats was 8.6±1.4%, representing a relative weight loss of 13.8±1.4% compared to the control group. In conclusion, Tesofensine is a potent triple monoamine reuptake inhibitor that effectively induces hypophagia and weight loss in obese animal models.
Keywords
Tesofensine, 195875-84-4, NS-2330, NS2330, NS 2330, Dopamine Transporter, Serotonin Transporter, DAT, SLC6A3, 5-HTT, SERT, SLC6A4, triple monoamine reuptake, neurotransmitters dopamine, norepinephrine, serotonin, anti-obesity agent, Inhibitor, inhibitor, inhibit
References
[1] Lieuwe Appel, et al. Tesofensine, a novel triple monoamine re-uptake inhibitor with anti-obesity effects: dopamine transporter occupancy as measured by PET. Eur Neuropsychopharmacol. 2014 Feb;24(2):251-61.
[2] Ann A Coulter, et al. Centrally Acting Agents for Obesity: Past, Present, and Future. Drugs. 2018 Jul;78(11):1113-1132.
[3] Anne Marie D Axel, et al. Tesofensine, a novel triple monoamine reuptake inhibitor, induces appetite suppression by indirect stimulation of alpha1 adrenoceptor and dopamine D1 receptor pathways in the diet-induced obese rat.Neuropsychopharmacology. 2010 Jun;35(7):1464-76.
**Background**
Fluorescent labeling is a fundamental tool in biomedical research, enabling the visualization and tracking of biomolecules within complex biological systems. Among various labeling strategies, bioorthogonal chemistry has emerged as a powerful approach, allowing for the selective modification of molecules in vivo or in vitro without interfering with native biological processes. Specifically, the azide-alkyne cycloaddition, often referred to as “click chemistry,” provides a highly efficient and stable method for attaching fluorophores to target proteins, lipids, or nucleic acids. This technology is particularly valuable in the development of functionalized nanobodies and the study of protein-protein interactions. In this context, we will introduce a potent fluorescent dye for these applications – Cyanine5 azide.
**Definition**
Cyanine5 azide is a fluorescent dye containing an azide group, characterized by an excitation wavelength ($\lambda_{ex}$) of 647 nm and an emission wavelength ($\lambda_{em}$) of 668 nm.
**Mechanism of Action**
According to the Cyanine5 azide description, this compound is designed for versatile conjugation via click chemistry. It contains a reactive azide group that can undergo a copper-catalyzed azide-alkyne cycloaddition (CuAAC) when reacted with terminal alkynes. Additionally, it can participate in ring strain-promoted alkyne-azide cycloaddition (SPAAC) with molecules containing dibenzocyclooctyne (DBCO) or bicyclo[6.1.0]nonyne (BCN) groups. This dual reactivity allows researchers to choose between copper-dependent and copper-free labeling methods depending on the sensitivity of their biological sample. For those seeking detailed Cyanine5 azide technical information, the compound possesses a molecular weight of 601.22 and a chemical formula of $\text{C}_{35}\text{H}_{45}\text{ClN}_6\text{O}$.
**Experimental Applications**
The utility of Cyanine5 azide has been demonstrated in advanced chemical synthesis and biological labeling. In studies regarding the total chemical synthesis of a functionalized GFP nanobody, the dye was employed to introduce fluorescence into the protein structure. When evaluating Cyanine5 azide in vitro, the dye’s strong emission in the far-red spectrum (662-668 nm) ensures minimal background interference and high signal-to-noise ratios in imaging experiments. The ability to precisely label nanobodies allows for the detailed study of target recognition and binding kinetics. In conclusion, Cyanine5 azide is a potent and versatile fluorescent probe for bioorthogonal labeling and imaging research.
Keywords
Cyanine5 azide, 1267539-32-1, Fluorescent Dye, fluorescent dye, copper-catalyzed click reaction, azide, NIR live organism imaging, Inhibitor, inhibitor, inhibit
References
**Background**
Hypertension and angina pectoris are prevalent cardiovascular conditions characterized by elevated blood pressure and reduced myocardial oxygen supply, respectively. These conditions often lead to severe complications, including myocardial infarction and heart failure, making the regulation of the adrenergic system a primary therapeutic target. The β1-adrenergic receptor plays a critical role in modulating heart rate and contractility; therefore, selective blockade of this receptor can effectively reduce cardiac workload and stabilize blood pressure. In this context, we will introduce a cardioselective β1-adrenergic receptor blocker – Atenolol.
**Definition**
Atenolol is a cardioselective β1-adrenergic receptor blocker with a Ki of 697 nM at the β1-adrenoceptor in guinea pig left ventricle membrane. According to the Atenolol technical information, it is used extensively in the research of hypertension and angina pectoris.
**In Vitro and In Vivo Studies**
The Atenolol biological activity has been demonstrated across various experimental models. In vitro studies indicate that Atenolol (1-100 μM, 5 h) strengthens the inhibitory effect on the migration of rat aortic smooth muscle cells when combined with Nifedipine (1-100 μM). Furthermore, Atenolol (1-100 μM) inhibited cell proliferation in rat aortic smooth muscle cells, with a 20% reduction observed after 72 h of incubation at 100 μM. In hemangioma-derived endothelial cells (Hem-ECs), Atenolol (50-150 μM, 24 h) decreased cell survival in a dose-dependent manner. Notably, research into Atenolol Autophagy showed that treatment with 100 μM for 6 h increased the LC3-Ⅱ/LC3-Ⅰ ratio and decreased p62 in Hem-ECs.
Atenolol in vivo studies have further validated its efficacy. In 2K1C renovascular hypertensive rats, the combination of Atenolol (5-20 mg/kg, i.g., single dose) and Amlodipine reduced and stabilized blood pressure within 24 h. In an Hras5 tumor xenograft rat model, Atenolol (6 mg/kg, p.o., single dose) combined with Nifedipine abolished the hypertensive and tachycaidic effects induced by ZD6126. Additionally, chronic administration of Atenolol (40 mg/kg, p.o., daily for 6 weeks) in male Wistar rats increased the density of plasma membrane β1- and β2-adrenoceptors while decreasing β1-adrenoceptor mRNA expression. In conclusion, Atenolol is a potent cardioselective β1-blocker effective for modulating cardiovascular function and cell behavior.
Keywords
Atenolol, 29122-68-7, (RS)-Atenolol, Adrenergic Receptor, Beta Receptor, Hypertension, angina pectoris, β1-adrenergic receptor, cardioselective, Hem-ECs, Inhibitor, inhibitor, inhibit
References
[1] Heel RC, et al. Atenolol: a review of its pharmacological properties and therapeutic efficacy in angina pectoris and hypertension. Drugs. 1979;17(6):425-460.
[2] Engel G, et al. (+/-)[125Iodo] cyanopindolol, a new ligand for beta-adrenoceptors: identification and quantitation of subclasses of beta-adrenoceptors in guinea pig. Naunyn Schmiedebergs Arch Pharmacol. 1981;317(4):277-285.
[3] Corsini A, et al. Effect of the nifedipine-atenolol association on arterial myocyte migration and proliferation. Pharmacol Res. 1993 May-Jun;27(4):299-307.
[4] Lorusso B, et al. Β-blockers activate autophagy on infantile hemangioma-derived endothelial cells in vitro. Vascul Pharmacol. 2022 Oct;146:107110
[5] Shen FM, et al. Synergistic effects of atenolol and amlodipine for lowering and stabilizing blood pressure in 2K1C renovascular hypertensive rats. Acta Pharmacol Sin. 2005 Nov;26(11):1303-8.
[6] Gould S, et al. Effect of pretreatment with atenolol and nifedipine on ZD6126-induced cardiac toxicity in rats. J Natl Cancer Inst. 2007 Nov 21;99(22):1724-8.
[7] Horinouchi T, et al. Different changes of plasma membrane beta-adrenoceptors in rat heart after chronic administration of propranolol, atenolol and bevantolol. Life Sci. 2007 Jul 12;81(5):399-404.
**Background**
Fatty amides are a diverse group of lipid-derived compounds that play significant roles in various biological processes, including cell signaling, membrane stabilization, and the modulation of inflammatory responses. These molecules often serve as precursors or metabolites in the synthesis of bioactive lipids, which are critical for maintaining cellular homeostasis and regulating physiological functions. Understanding the structural properties and biological interactions of primary fatty amides is essential for advancing research in lipid biochemistry and pharmacology. In this context, we will introduce a primary fatty amide – Decanamide.
**Definition**
Decanamide is a primary fatty amide characterized by a ten-carbon chain. According to the Decanamide technical information, it possesses a molecular weight of 171.28 and a chemical formula of C10H21NO.
**Structural Characteristics**
The Decanamide description identifies it as a primary fatty amide. Research into its physical properties has focused heavily on its molecular arrangement and crystallization. Specifically, the crystal structure of decanamide has been analyzed to determine its spatial configuration and intermolecular bonding patterns, which are fundamental to understanding its Decanamide biological activity in various experimental settings. In conclusion, Decanamide is a primary fatty amide utilized as a tool in lipid research and structural biology.
Keywords
Decanamide, 2319-29-1, Biochemical Assay Reagents, Inhibitor, inhibitor, inhibit
References
[1] J. R. Brathovde, et al. The crystal structure of decanamide. Acta Cryst. (1958). 11, 729-732.
**Background**
Schizophrenia is a severe and chronic mental disorder characterized by distortions in thinking, perception, emotions, and behavior. For decades, the primary pharmacological approach to treating schizophrenia has focused on the blockade of dopamine D2 receptors and serotonin 5-HT2A receptors. While effective for positive symptoms, these traditional antipsychotics often lead to significant side effects, including extrapyramidal symptoms and metabolic disturbances. Consequently, there is a critical need for novel therapeutic agents with alternative mechanisms of action that can provide antipsychotic effects without the burden of D2-related adverse events. In this context, we will introduce a unique psychotropic agent – (Rac)-Ulotaront.
**Definition**
(Rac)-Ulotaront (also known as (Rac)-SEP-363856 hydrochloride) is an orally active and CNS-active psychotropic agent that exerts antipsychotic-like effects through a unique, non-D2/5-HT2A mechanism of action.
**In Vitro and In Vivo Studies**
The (Rac)-Ulotaront description highlights its potential as a breakthrough treatment for schizophrenia due to its distinct pharmacological profile. According to the (Rac)-Ulotaront biological activity, this compound does not rely on the traditional dopamine D2 receptor antagonism to achieve its therapeutic effects, thereby potentially reducing the risk of motor side effects. The (Rac)-Ulotaront formula is C9H14ClNOS with a molecular weight of 219.73. Research indicates that (Rac)-Ulotaront is capable of crossing the blood-brain barrier to exert its effects within the central nervous system. In vivo studies have demonstrated that this agent possesses antipsychotic-like properties, supporting its development as a novel treatment for patients with schizophrenia who are unresponsive to or intolerant of current medications. In conclusion, (Rac)-Ulotaront is a novel psychotropic agent that offers a promising non-D2 receptor-based strategy for the treatment of schizophrenia.
Keywords
(Rac)-Ulotaront, 1310422-02-6, (Rac)-SEP-363856, (Rac)-SEP-856, 5-HT Receptor, Serotonin Receptor, 5-hydroxytryptamine Receptor, Inhibitor, inhibitor, inhibit
References
**Background**
Chronic inflammation and oxidative stress are central drivers in the pathogenesis of various metabolic and infectious diseases. In particular, secondary diabetic complications often arise from prolonged hyperglycemia, leading to tissue damage and systemic dysfunction. Furthermore, the inflammatory response, often characterized by the overproduction of nitric oxide (NO) and pro-inflammatory mediators, plays a critical role in the progression of infectious diseases, including HIV and COVID-19. Managing these pathways is essential for reducing tissue injury and improving clinical outcomes. In this context, we will introduce a potent antioxidative and anti-inflammatory agent – Benfotiamine.
**Definition**
Benfotiamine (S-Benzoylthiamine O-monophosphate) is a lipid-soluble derivative of vitamin B1 that exhibits potent antioxidative and anti-inflammatory activity. According to the Benfotiamine description, it is utilized extensively in the research of diabetic complications and infectious diseases.
**In Vitro and In Vivo Studies**
The Benfotiamine biological activity has been demonstrated across various experimental models. In vitro studies using BV-2 microglial cells showed that Benfotiamine (50-250 μM; pretreated for 30 min and then exposed to LPS for 24 h) decreases LPS-induced production of NO by suppressing iNOS-mRNA and protein levels. Additionally, when pretreated for 30 min and exposed to LPS for 6 h, Benfotiamine (50-250 μM) suppresses the mRNA expression of PTGS and the protein expression of COX-2 in BV2 cells. These results highlight its potential to attenuate inflammatory responses in microglia.
Regarding Benfotiamine In Vivo application, research indicates that Benfotiamine (100 mg/kg; i.p. for 14 d) effectively alleviates cerebral oxidative damage in FVB mice induced by streptozotocin (STZ). This protective effect occurs independently of advanced glycation end-products, tissue factor, and TNF-alpha. For researchers requiring specific Benfotiamine technical information, such as the Benfotiamine Formula (C19H23N4O6PS) or molecular weight (466.45), these parameters are critical for calculating precise experimental dosages. In conclusion, Benfotiamine is a versatile vitamin B1 derivative that serves as a powerful tool for studying the mitigation of oxidative damage and inflammation.
Keywords
Benfotiamine, 22457-89-2, S-Benzoylthiamine O-monophosphate, HIV, SARS-CoV, Human immunodeficiency virus, SARS coronavirus, food, supplement, diabetic, complications, antioxidative, Inhibitor, inhibitor, inhibit
References
[1] Allowitz KV, et, al. Therapeutic potential of vitamin B1 derivative benfotiamine from diabetes to COVID-19. Future Med Chem. 2022 Jun;14(11):809-826.
[2] Bozic I, et, al. Benfotiamine attenuates inflammatory response in LPS stimulated BV-2 microglia. PLoS One. 2015 Feb 19;10(2):e0118372.
[3] Wu S, et, al. Benfotiamine alleviates diabetes-induced cerebral oxidative damage independent of advanced glycation end-product, tissue factor and TNF-alpha. Neurosci Lett. 2006 Feb 13;394(2):158-62.
**Background**
The assessment of dietary protein intake, specifically the consumption of animal-derived meats, is critical for nutritional epidemiology and the study of metabolic disorders. While self-reported dietary logs are common, they are often subject to recall bias and inaccuracy. Consequently, there is a significant need for objective biochemical markers that can accurately reflect exogenous protein intake. Certain metabolites, such as methylhistidines, serve as reliable biomarkers because they are not synthesized in significant quantities by the human body and are excreted in the urine. In this context, we will introduce an objective indicator of meat ingestion – 1-Methyl-L-histidine.
**Definition**
1-Methyl-L-histidine is a human endogenous metabolite with the molecular formula C7H11N3O2 and a molecular weight of 169.18. It serves as a qualitative indicator for the intake of meats from various sources and the exogenous consumption of 3-methylhistidine (3MH).
**In Vivo Studies**
According to the 1-Methyl-L-histidine description, this compound is naturally present in various types of meats. Research focusing on 1-Methyl-L-histidine in vivo has demonstrated that its urinary excretion increases significantly following the intake of meat. This makes the compound a valuable tool for researchers monitoring dietary patterns and their effects on endocrine diseases, nervous system disorders, and cardiovascular system disorders. For researchers seeking detailed 1-Methyl-L-histidine technical information, it is noted that the compound is classified structurally under ketones, aldehydes, and acids. In conclusion, 1-Methyl-L-histidine is a reliable endogenous metabolite used as a biomarker for meat ingestion and exogenous 3-methylhistidine intake.
Keywords
1-Methyl-L-histidine, 332-80-9, Endogenous Metabolite, 3-methylhistidine, meats, Inhibitor, inhibitor, inhibit
References