Clobetasol propionate is a CYP3A5 inhibitor for dermatoses research
**Background**
Cytochrome P450 (CYP) enzymes play a critical role in the metabolism of a wide array of endogenous compounds and exogenous drugs. Among these, the CYP3A subfamily is the most abundant and significant in the human liver and intestines. While CYP3A4 is the predominant isoform, CYP3A5 exhibits significant genetic polymorphism, and its expression levels vary greatly among individuals, influencing drug response and toxicity. Understanding the selective inhibition of these isoforms is essential for pharmacological research and personalized medicine. Additionally, corticosteroids have long been utilized in the treatment of inflammatory skin conditions, such as psoriasis and other dermatoses, due to their potent anti-inflammatory properties. In this context, we will introduce a selective CYP3A5 inhibitor and corticosteroid – Clobetasol propionate.
**Definition**
Clobetasol propionate is a potent and selective CYP3A5 inhibitor with an IC50 value of 0.206 μM.
**In Vitro and In Vivo Studies**
According to the Clobetasol propionate description, this compound acts as a heme-mediated selective inhibitor of human CYP3A5. Clobetasol propionate in vitro studies demonstrate that it possesses an IC50 of 15.6 μM for CYP3A4, indicating high selectivity for the 3A5 isoform. In human AsPC-1 cells, the compound (1 μM; 24 hours) selectively inhibits CYP3A5 without increasing the protein levels of CYP3A4. Furthermore, it does not affect cell growth across various cell lines, including AsPC-1 wild-type (WT), AsPC-1 CYP3A5–/– cells with CYP3A5 overexpression, and AsPC-1 CYP3A5–/– cells with CYP3A4 overexpression. Specific cellular effects in AsPC-1 cells showed IC50 values ranging from 0.021 μM (doxycycline-induced CYP3A5 overexpressing) to 0.103 μM (CRISPR/Cas9-mediated CYP3A5 knock-out with doxycycline-induced overexpression). Additionally, in Sf21 cells, it inhibited human BSEP with an IC50 of 8.5 μM and rat Bsep with an IC50 of 35 μM.
Regarding Clobetasol propionate In Vivo activity, the compound was applied topically on a daily basis for 14 days in a human psoriatic skin-SCID mouse transplant model. The results indicated a significant reduction in the epidermal thickness of both normal and psoriatic skin. This Clobetasol propionate biological activity underscores its potential for research into psoriasis and other dermatological disorders. In conclusion, Clobetasol propionate is a selective CYP3A5 inhibitor and a potent corticosteroid suitable for dermatological and metabolic research.
Keywords
Clobetasol propionate, 25122-46-7, Cytochrome P450, CYPs, corticosteroid, psoriasis, dermatoses, Inhibitor, inhibitor, inhibit
References
[1] William C Wright, et al. Clobetasol Propionate Is a Heme-Mediated Selective Inhibitor of Human Cytochrome P450 3A5. J Med Chem. 2020 Feb 13;63(3):1415-1433.
[2] Steven R Feldman, et al. Topical clobetasol propionate in the treatment of psoriasis: a review of newer formulations. Am J Clin Dermatol. 2009;10(6):397-406.
[3] M Zeigler, et al. Anti-CD11a ameliorates disease in the human psoriatic skin-SCID mouse transplant model: comparison of antibody to CD11a with Cyclosporin A and clobetasol propionate. Lab Invest. 2001 Sep;81(9):1253-61.
**Background**
Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase that can undergo rearrangement, leading to the expression of EML4-ALK fusion proteins. This oncogenic driver is frequently found in a subset of non-small-cell lung cancers (NSCLC), where it promotes tumor cell proliferation, survival, and metastasis. Due to its critical role in driving malignancy, ALK has become a primary therapeutic target for the development of precision medicines in lung cancer. However, the emergence of resistant mutations, such as the gatekeeper mutation, often limits the long-term efficacy of first-generation inhibitors. Furthermore, the ability of a drug to penetrate the blood-brain barrier is essential for treating CNS metastases, which are common in ALK-positive patients. In this context, we will introduce a potent and selective ALK inhibitor – Alectinib.
**Definition**
Alectinib is a potent, selective, and orally available ALK inhibitor with an IC50 of 1.9 nM and a Kd value of 2.4 nM in an ATP-competitive manner. According to the Alectinib description, it also effectively inhibits the resistant mutants ALK F1174L and ALK R1275Q with IC50 values of 1 nM and 3.5 nM, respectively.
**In Vitro and In Vivo Studies**
The Alectinib biological activity has been extensively validated across various models. In Alectinib in vitro studies, treatment with concentrations ranging from 0 to 1000 nM for 2 hours in NCI-H2228 cells expressing EML4-ALK prevented the autophosphorylation of ALK and substantially suppressed the phosphorylation of STAT3 and AKT. Additionally, treatment with 0-1000 nM Alectinib for 5 days reduced cell activity in a dose-dependent manner in HCC827, A549, and NCIH522 cell lines.
Regarding Alectinib In Vivo efficacy, SCID or nude mice bearing NCI-H2228 cells were administered Alectinib orally once daily for 11 days at doses ranging from 0.2 to 20 mg/kg. This treatment resulted in dose-dependent tumor growth inhibition, with an EC50 of 0.46 mg/kg, and led to tumor regression. Notably, no significant differences in body weight or gross signs of toxicity were observed at any dose level. Furthermore, Alectinib demonstrates effective central nervous system (CNS) penetration, making it a valuable tool for Alectinib Cancer research. In conclusion, Alectinib is a highly potent and selective ALK inhibitor capable of overcoming resistant mutations and penetrating the CNS.
Keywords
Alectinib, 1256589-74-8, CH5424802, RO5424802, AF-802, CH 5424802, CH-5424802, RO 5424802, RO-5424802, AF802, AF 802, Anaplastic lymphoma kinase (ALK), Anaplastic lymphoma kinase, ALK tyrosine kinase receptor, CD246
References
[1] Sakamoto H, et al. CH5424802, a selective ALK inhibitor capable of blocking the resistant gatekeeper mutant. Cancer Cell. 2011, 19(5), 679-690.
[2] Gadgeel S, et al. Alectinib versus crizotinib in treatment-naive anaplastic lymphoma kinase-positive (ALK+) non-small-cell lung cancer: CNS efficacy results from the ALEX study. Ann Oncol. 2018 Nov 1;29(11):2214-2222.
**Background**
The sigma-1 receptor ($\sigma_1$R) is a unique chaperone protein located primarily in the endoplasmic reticulum membrane, playing a critical role in modulating calcium signaling, protein folding, and cellular stress responses. Due to its widespread expression in the central and peripheral nervous systems, $\sigma_1$R has become a significant target for treating various neurological and respiratory disorders. In particular, the modulation of $\sigma_1$R is closely linked to the regulation of the cough reflex and bronchial smooth muscle tone. Agents that target this receptor can provide potent antitussive and spasmolytic effects, making them valuable for managing airway resistance and bronchial interceptions. In this context, we will introduce a potent sigma-1 receptor agonist – Pentoxyverine.
**Definition**
Pentoxyverine (Carbetapentane) citrate is an orally active, blood-brain barrier permeable sigma-1 receptor agonist and muscarinic antagonist. According to the Pentoxyverine technical information, it exhibits $K_i$ values of 41 nM for $\sigma_1$, 894 nM for $\sigma_2$, and 75 nM for guinea-pig brain membrane $\sigma_1$.
**In Vitro and In Vivo Studies**
The Pentoxyverine biological activity is characterized by its ability to act as a potent antitussive, anticonvulsant, and spasmolytic agent. In vivo studies have demonstrated its complex role in nociception and respiratory control. In a model using female wild-type mice (25-30 g), Pentoxyverine (0.5, 1, 2, 4, 8, 16, 32 mg/kg; SC) administered 30 minutes before intraplantar capsaicin (0.125 $\mu$g) dose-dependently potentiated the sensitizing effect of capsaicin to mechanical stimuli. Specifically, a dose of 16 mg/kg (SC) showed strong potentiation of capsaicin-induced secondary mechanical allodynia. Furthermore, Pentoxyverine in vivo data indicates that oral administration of 50 mg/kg for 7 days in mice (22-25 g) significantly increased the latent period of aqueous ammonia-induced cough by 121.72% and inhibited cough frequency by 45.45% when used as a positive control. These results highlight its efficacy in weakening the cough reflex and promoting bronchial smooth muscle relaxation. In conclusion, Pentoxyverine is a potent $\sigma_1$ receptor agonist with significant potential for research into respiratory and nociceptive modulation.
Keywords
Pentoxyverine, 23142-01-0, Carbetapentane, Sigma Receptor, mAChR, Muscarinic acetylcholine receptor, sigma-1 receptor, σ1, σ2, muscarinic, antitussive, anticonvulsant, spasmolytic, bronchial interceptor, cough reflex, bronchial smooth muscle relaxation, airway resistance, Inhibitor, inhibitor, inhibit
References
[1] Mohamed SH, et, al. Extraction-free spectrophotometric assay of the antitussive drug pentoxyverine citrate using sulfonephthalein dyes. Spectrochim Acta A Mol Biomol Spectrosc. 2019 Nov 5;222:117186.
[2] Calderon SN, et, al. Novel 1-phenylcycloalkanecarboxylic acid derivatives are potent and selective sigma 1 ligands. J Med Chem. 1994 Jul 22;37(15):2285-91.
[3] Brown C, et, al. Antitussive activity of sigma-1 receptor agonists in the guinea-pig. Br J Pharmacol. 2004 Jan;141(2):233-40.
[4] J M Entrena, et al. Sigma-1 Receptor Agonism Promotes Mechanical Allodynia After Priming the Nociceptive System with Capsaicin. Sci Rep. 2016 Nov 25:6:37835. doi: 10.1038/srep37835.
[5] Yuebin Ge, et al. In Vivo Evaluation of the Antiasthmatic, Antitussive, and Expectorant Activities and Chemical Components of Three Elaeagnus Leaves. Evid Based Complement Alternat Med. 2015:2015:428208.
**Background**
Breast cancer remains one of the most prevalent and lethal malignancies among women worldwide. A critical challenge in cancer therapy is the evasion of apoptosis, a programmed cell death process that is often suppressed in tumor cells to allow for uncontrolled proliferation and survival. The Bcl-2 family of proteins plays a central role in regulating this process, with Bax (Bcl-2-associated X protein) acting as a key pro-apoptotic member. Upon activation, Bax inserts into the mitochondrial outer membrane, leading to mitochondrial outer membrane permeabilization (MOMP) and the subsequent release of cytochrome c into the cytosol, which triggers the caspase cascade. Therefore, developing small molecules that can directly activate Bax represents a promising strategy for overcoming apoptosis resistance in GL0388 Cancer research. In this context, we will introduce a potent Bax activator – GL0388.
**Definition**
GL0388 is a Bax activator that promotes the insertion of Bax into the mitochondrial membrane, exhibiting antiproliferative activities against various cancer cells with $\text{IC}_{50}$ values ranging from 0.299 to 1.57 $\mu\text{M}$.
**In Vitro and In Vivo Studies**
According to the GL0388 description, this compound is a 2-fluoro-fluorene derivative designed for the treatment of breast cancer. GL0388 in vitro studies demonstrated that the compound (0.1-10 $\mu\text{M}$; 72 h) significantly inhibits the proliferation of MDA-MB-231 and MCF-7 breast cancer cell lines, with $\text{IC}_{50}$ values of 0.96 $\mu\text{M}$ and 0.52 $\mu\text{M}$, respectively. Furthermore, GL0388 (0.01-100 $\mu\text{M}$) showed broad antiproliferative effects across 60 human tumor cell lines, with $\text{GI}_{50}$ values between 0.299 and 1.57 $\mu\text{M}$. Mechanistically, GL0388 (1-10 $\mu\text{M}$; 24 h) promotes the dose-dependent insertion of Bax into the mitochondrial membranes of MDA-MB-231 cells, increasing cytosolic cytochrome c levels. Additionally, treatment with GL0388 (1-10 $\mu\text{M}$; 48 h) significantly upregulates cleaved PARP-1 and cleaved caspase 3, while concentrations of 0.1-1 $\mu\text{M}$ for 24 h inhibit colony formation and invasion.
Regarding GL0388 in vivo efficacy, the compound was evaluated in female nude mice bearing MDA-MB-231 xenografts. Administration of GL0388 (10-20 mg/kg via i.p. or 15 mg/kg via i.t. once daily for 10 days) dose-dependently suppressed tumor growth. Notably, i.t. administration at 15 mg/kg every other day achieved an inhibition rate of 55%, which was comparable to the efficacy of daily i.p. administration at 20 mg/kg. In conclusion, GL0388 is a potent Bax activator that induces Bax-mediated apoptosis and suppresses tumor growth in breast cancer models.
Keywords
GL0388, 2886772-68-3, GL 0388, GL-0388, Bcl-2 Family, Bax, mitochondrial, antiproliferative, apoptosis, tumor, Inhibitor, inhibitor, inhibit
References
**Background**
Aplastic anemia is a severe bone marrow failure syndrome characterized by pancytopenia and a significant reduction in hematopoietic stem cells. This condition leads to a critical deficiency in white blood cells, red blood cells, and platelets, increasing the risk of life-threatening infections and hemorrhage. Research into agents that can promote hematopoiesis and thrombopoiesis is essential for developing effective therapeutic strategies to restore blood cell counts and improve patient outcomes. In this context, we will introduce an orally active green pigment and antioxidant – Chlorophyllin sodium copper salt.
**Definition**
Chlorophyllin sodium copper salt is an orally active green pigment, antioxidant, and antimutagenic agent that promotes hematopoiesis and thrombopoiesis. According to the Chlorophyllin sodium copper salt technical information, it possesses a molecular weight of 724.15 and the chemical formula C34H31CuN4Na3O6.
**In Vivo Studies**
The Chlorophyllin sodium copper salt biological activity has been evaluated in various models to determine its efficacy in blood cell recovery. In vivo studies using aplastic anemic BALB/c mice demonstrated that the administration of Chlorophyllin sodium copper salt (25, 50, and 100 mg/kg/day) via gastrogavage for 20 days significantly impacted blood parameters. Specifically, the medium and high doses were found to increase peripheral blood white cell and platelet counts. Furthermore, in T cell-MSC cocultures, the percentage of Forkhead box protein 3 (FOXP3+) T cells was increased, and the cytokine transforming growth factor β1 was up-regulated. In conclusion, Chlorophyllin sodium copper salt is a potent agent that supports the recovery of hematopoietic functions and modulates immune responses in models of aplastic anemia.
Keywords
Chlorophyllin sodium copper, 11006-34-1, Biochemical Assay Reagents, Orally, green pigment, antioxidant, antimutagenic, hematopoiesis, thrombopoiesis, Inhibitor, inhibitor, inhibit
References
[1] Li-Ming Yin, et al. Effects of sodium copper chlorophyllin on mesenchymal stem cell function in aplastic anemia mice. Chin J Integr Med. 2013 May;19(5):360-6.
[2] Sanja M. Petrovic, et al. Chlorophyllin sodium copper salt in hydrogel formulations: spectrophotometric stability studies and in vitro release. Chemical Papers. Volume 77, pages 2635–2645, (2023).
**Background**
Phospholipase A2 (PLA2) is a critical enzyme that catalyzes the hydrolysis of phospholipids, releasing arachidonic acid and other lipid mediators that play pivotal roles in inflammatory responses and cellular signaling. In plant biology, the regulation of microtubule arrays is essential for maintaining structural integrity and guiding root growth. Disruptions in these processes can significantly impact plant development and survival. Given the importance of PLA2 inhibition in modulating both inflammatory pathways in mammals and growth mechanisms in plants, researchers seek potent derivatives to study these biological processes. In this context, we will introduce a derivative of aristolochic acid – Aristolochic acid C.
**Definition**
Aristolochic acid C is a monophenol derivative of aristolochic acid that acts as a phospholipase A2 (PLA2) inhibitor. According to the Aristolochic acid C technical information, this compound is utilized to study the inhibition of inflammatory mediators and the disruption of cortical microtubule arrays.
**In Vitro Studies**
Aristolochic acid C is characterized by the molecular formula C16H9NO7 and a molecular weight of 327.25. Regarding the Aristolochic acid C biological activity, in vitro studies have evaluated its anti-inflammatory potential in human neutrophils. Specifically, the compound demonstrated an IC50 > 10 μg/mL when assessing the inhibition of fMLP/CB-induced elastase release after 5 minutes. Similarly, it exhibited an IC50 > 10 μg/mL in the inhibition of fMLP/CB-induced superoxide anion generation after 5 minutes. Beyond human cell lines, research into the Aristolochic acid C description indicates that as a PLA2 inhibitor, it is capable of disrupting cortical microtubule arrays and inhibiting root growth in Arabidopsis. In conclusion, Aristolochic acid C is a PLA2 inhibitor with potential applications in studying inflammatory responses and plant developmental biology.
Keywords
Aristolochic acid C, 4849-90-5, Phospholipase, Inhibitor, inhibitor, inhibit
References
**Background**
Growth hormone (GH) plays a critical role in maintaining metabolic homeostasis and promoting growth throughout the human lifespan. The regulation of GH is primarily controlled by the hypothalamus, which secretes specific peptides to modulate the anterior pituitary gland. Among these, the growth hormone-releasing hormone (GHRH) is essential for the synthesis and secretion of GH from pituitary somatotropes. Dysregulation of this axis is often associated with metabolic disorders, including diabetes, making the study of GHRH signaling a focal point for endocrine research. In this context, we will introduce a potent hypothalamic polypeptide – Human growth hormone-releasing factor.
**Definition**
Human growth hormone-releasing factor is a hypothalamic polypeptide that stimulates the production and release of growth hormone by binding to the GHRH receptor (GHRHR) on cells in the anterior pituitary. According to the Human growth hormone-releasing factor description, this peptide consists of a specific 44-amino acid sequence (YADAIFTNSYRKVLGQLSARKLLQDIMSRQQGESNQERGARARL-NH2) with a molecular weight of 5039.65 (free base).
**Mechanism of Action**
The GHRHR is a member of the class II B GPCR family, which predominantly couples to the Gs-adenylate cyclase-cAMP signaling pathway. Human growth hormone-releasing factor In Vitro activity is characterized by its ability to activate these receptors, mirroring the action of other peptide hormones such as secretin, glucagon-like peptides, and vasoactive intestinal peptide. Expressed in the arcuate nucleus of the hypothalamus and released into the portal vasculature, the peptide directly stimulates growth hormone synthesis. Researchers seeking detailed Human growth hormone-releasing factor technical information can observe that this activation is central to the regulation of somatotrope function.
**Experimental Application**
The biological utility of this peptide is well-documented in endocrine studies. By utilizing the Human growth hormone-releasing factor biological activity, researchers can investigate the interplay between GHRH and metabolic diseases. For instance, studies have explored the role of growth hormone-releasing hormone in the context of diabetes to understand how GH deficiency or excess impacts glucose metabolism. The peptide’s precise Human growth hormone-releasing factor Formula (C 215 H 358 N 72 O 66 S.xC 2 HF 3 O 2) ensures high specificity for the GHRHR, allowing for accurate modeling of the hypothalamic-pituitary-somatotropic axis. In conclusion, Human growth hormone-releasing factor is a critical tool for studying the stimulation of growth hormone production and its implications in metabolic health.
Keywords
Human growth hormone-releasing factor, Growth Hormone Releasing Factor human, Somatorelin (1-44) amide (human), GHSR, Growth hormone secretagogue receptor, Ghrelin receptor, Hypothalamic, peptide, growth, hormone, Inhibitor, inhibitor, inhibit
References
**Background**
The p38 mitogen-activated protein kinase (MAPK) pathway plays a critical role in the regulation of cellular responses to various external stimuli, including inflammatory cytokines, osmotic stress, and ultraviolet radiation. In particular, p38 MAPK is essential for the production of pro-inflammatory cytokines and the activation of several downstream enzymes involved in the inflammatory cascade. One such enzyme is the tumor necrosis factor $\alpha$-converting enzyme (TACE), also known as ADAM-17, which is responsible for the shedding of membrane-bound TNF-$\alpha$ into its soluble, active form. Dysregulation of the p38-TACE axis is often associated with chronic inflammatory diseases and autoimmune disorders. Therefore, developing highly specific inhibitors of p38 is of significant research interest for controlling excessive inflammation. In this context, we will introduce a p38 inhibitor – EO 1428.
**Definition**
EO 1428 is a highly specific inhibitor of p38 belonging to the aminobenzophenone class. According to the EO 1428 description, this compound is designed to target p38 MAPK to attenuate inflammatory responses.
**In Vitro Studies**
The EO 1428 biological activity has been demonstrated through its ability to modulate cytokine production and enzyme activity. In terms of chemical properties, the EO 1428 formula is $\text{C}_{20}\text{H}_{16}\text{BrClN}_2\text{O}$ with a molecular weight of 415.71. In vitro studies using human peripheral blood mononuclear cells (PBMC) showed that EO 1428 exhibits potent anti-inflammatory activity. Specifically, it inhibits the production of LPS-induced TNF-alpha with an $\text{IC}_{50}$ value of 4 nM and inhibits the production of LPS-induced IL-beta with an $\text{IC}_{50}$ value of 14 nM. Furthermore, EO 1428 (1 $\mu$M) markedly attenuates the up-regulation of tumor necrosis factor $\alpha$-converting enzyme (TACE) activity induced by LPS in primary human monocytes. These results indicate that the compound effectively disrupts the p38-mediated activation of TACE. In conclusion, EO 1428 is a potent and specific p38 inhibitor that effectively suppresses the production of pro-inflammatory cytokines in human PBMC.
Keywords
EO 1428, 321351-00-2, EO1428, EO-1428, p38 MAPK, specific p38 inhibitor, tumor necrosis factor α-converting enzyme, TACE, Inhibitor, inhibitor, inhibit
References
**Background**
The c-myc protein is a well-known transcription factor that plays a pivotal role in the regulation of growth-related gene transcription, cell cycle progression, and apoptosis. Due to its ability to drive uncontrolled cellular proliferation, c-myc is frequently overexpressed in various malignancies and is considered a primary driver of oncogenesis. In particular, the role of c-myc in the growth of human breast cancer has been extensively documented, making it a critical target for therapeutic intervention and molecular study. Understanding the interactions of the c-myc protein is essential for developing strategies to inhibit tumor growth. In this context, we will introduce a synthetic tool for studying this protein – c-Myc Peptide.
**Definition**
c-Myc Peptide is a synthetic peptide corresponding to the C-terminal amino acids (410-419) of the human c-myc protein, with the sequence Glu-Gln-Lys-Leu-Ile-Ser-Glu-Glu-Asp-Leu (EQKLISEEDL).
**In Vitro Studies**
According to the c-Myc Peptide description, this peptide serves as a representative fragment of the human c-myc protein involved in transcriptional regulation. Regarding c-Myc Peptide in vitro activity, research indicates that c-myc plays a critical role in the growth of breast cancer cells. Specifically, studies utilizing phosphorothioate antisense oligonucleotides to inhibit c-myc expression have identified its essential role in the proliferation of human breast cancer cell lines. The c-Myc Peptide formula (C53H87F3N12O23) and its molecular weight of 1317.32 ensure high specificity for research applications involving the C-terminal region of the protein. This peptide is particularly useful for researchers investigating c-Myc Peptide Cancer mechanisms and the regulation of growth-related genes. In conclusion, c-Myc Peptide is a synthetic C-terminal fragment of human c-myc used to study the regulation of gene transcription and cancer cell growth.
Keywords
c-Myc Peptide, 2918768-02-0, c-Myc, Myc, Inhibitor, inhibitor, inhibit
References
**Background**
Cancer remains one of the most challenging health crises globally, necessitating the discovery of novel preventive and therapeutic agents. Polyphenols, naturally occurring compounds found in various plants, have gained significant attention due to their diverse biological activities, including antioxidant, anti-inflammatory, and antitumor properties. Among these, catechins isolated from tea (Camellia sinensis) are particularly noted for their ability to modulate cell signaling pathways and inhibit tumor progression. Understanding the specific mechanisms by which these compounds exert their effects is crucial for developing effective cancer-preventive strategies. In this context, we will introduce a polyphenol with potent cancer-preventive activities – (-)-Gallocatechin gallate.
**Definition**
(-)-Gallocatechin gallate is a flavonoid and polyphenol isolated from tea that exhibits inhibitory effects on $\alpha$-Glucosidase and DPPH, with $\text{IC}_{50}$ values of 30.2 $\mu\text{M}$ and 12.2 $\mu\text{g/mL}$, respectively.
**In Vitro Studies**
The (-)-Gallocatechin gallate description highlights its role as a key bioactive component of tea. Regarding its distribution, research indicates that the amount of this compound does not differ significantly across leaves at different developmental stages, although its overall content remains relatively low. In terms of (-)-Gallocatechin gallate biological activity, studies have demonstrated that when combined with active catechins such as (-)-epigallocatechin gallate, it exerts synergistic effects on the induction of apoptosis and the inhibition of cell growth in PC-9 cells. Furthermore, in cellular assays using mouse 3T3-L1 cells, (-)-Gallocatechin gallate exhibited a potent inhibitory effect on G6PD-mediated NADPH production with an $\text{IC}_{50}$ value of 25 $\mu\text{M}$. These findings suggest that the compound can modulate metabolic pathways and trigger programmed cell death in specific cancer cell lines. In conclusion, (-)-Gallocatechin gallate is a natural polyphenol with significant potential for cancer research and metabolic inhibition.
Keywords
(-)-Gallocatechin gallate, 4233-96-9, (-)-Gallocatechol gallate, COMT, Catechol-O-methyltransferase, Inhibitor, inhibitor, inhibit
References
[1] Zhang LQ, et al. Accumulation of catechins and expression of catechin synthetic genes in Camellia sinensis at different developmental stages. Bot Stud. 2016 Dec;57(1):31.
[2] Zhou H, et al. C-geranylated flavanones from YingDe black tea and their antioxidant and α-glucosidase inhibition activities. Food Chem. 2017 Nov 15;235:227-233.