Main Research Findings
1) α-Estradiol was found to improve impaired cognitive functioning in animals with partial chronic deprivation of cholinergic functions in the central nervous system.

2) Treatment with α-estradiol inhibited progression of gastric cancer by acting on the GLI1 G-quadruplex.

Selected Data
1) The study by Lermontova et al was designed to investigate whether 17β-estradiol (17β-ED) and its stereoisomer 17α-estradiol (17α-ED) could improve learning and memory in rats with chronic cholinergic deficiency, an experimental model that mimics several pathological features of Alzheimer’s disease (AD). Previous studies had demonstrated that estrogens exert neuroprotective effects in models of cerebral ischemia and metabolic impairment, while epidemiological evidence suggested that higher estrogen levels are associated with a reduced risk of Alzheimer’s disease. However, it remained unclear whether these beneficial effects extended to chronic cholinergic degeneration, one of the hallmark pathological features of AD. The investigators therefore sought to compare the cognitive effects of the biologically active estrogen 17β-estradiol with those of its isomer 17α-estradiol, which possesses substantially weaker classical estrogenic activity but retains potent antioxidant properties. In addition to evaluating cognitive performance, the researchers examined the effects of both compounds on hormone-sensitive peripheral organs to determine whether improvements in learning were associated with endocrine activity or occurred independently of classical estrogen receptor stimulation [1].
Experiments were performed using adult male Wistar rats weighing between 180 and 200 grams. To eliminate variability arising from endogenous sex hormones, all animals were surgically castrated before the experimental procedures began. The rats were obtained from a standardized breeding colony and housed under controlled laboratory conditions throughout the study. Following recovery from castration, animals received daily subcutaneous injections of either 17β-estradiol or 17α-estradiol dissolved in oil. Hormone treatment began seven days before induction of cholinergic injury and continued for an additional ten to twelve days after lesioning, thereby ensuring that the animals were exposed to stable hormone concentrations throughout both the development of neuronal injury and the subsequent behavioral testing period. Two doses of each estrogen were investigated, 4 μg/kg and 40 μg/kg, allowing the investigators to evaluate possible dose-dependent effects on cognitive function and endocrine tissues. Separate control groups received vehicle (oil) injections instead of estrogen throughout the same treatment schedule.
To produce chronic cholinergic dysfunction resembling that observed in Alzheimer’s disease, the investigators employed the selective cholinergic neurotoxin AF64A. AF64A was freshly prepared immediately before administration from its precursor compound AF64 using Fisher’s established preparation method and diluted with artificial cerebrospinal fluid (CSF). Under ether anesthesia, experimental animals underwent stereotaxic intracerebroventricular injection of 3 nmol AF64A dissolved in 3 μL of artificial cerebrospinal fluid. This procedure selectively damaged cholinergic nerve terminals within the central nervous system while producing long-lasting impairment of cholinergic neurotransmission. Previous work had demonstrated that AF64A-induced degeneration is accompanied by persistent oxidative stress within the hippocampus and cerebral cortex, making this model particularly relevant for studying neuroprotective therapies in Alzheimer’s disease. One control group received identical intracerebroventricular injections of artificial cerebrospinal fluid without AF64A to provide normal baseline measurements for behavioral and physiological comparisons [1].
Behavioral testing was initiated ten to twelve days after intracerebral injection, allowing sufficient time for the development of stable cholinergic deficits. Learning and memory were assessed using the active avoidance paradigm in a shuttle box, a well-established behavioral task for evaluating associative learning. During each trial, rats were first presented with a light stimulus that served as the conditioned signal. If the animal crossed from the illuminated compartment into the adjacent dark compartment before delivery of a mild electric foot shock, the response was scored as a successful conditioned avoidance. Failure to move before shock administration resulted in an unconditioned escape response. The complete training session consisted of thirty-five stimulus presentations, providing repeated opportunities for animals to learn the association between the warning light and the impending aversive stimulus.
To distinguish learning acquisition from memory retention, behavioral performance was evaluated over two consecutive days. During the first day of testing, investigators calculated the mean percentage of successful conditioned avoidance responses during the final fifteen training trials, representing the animals’ ability to acquire the learned behavior after repeated exposure. On the second day, memory consolidation and retrieval were assessed by recording conditioned responses during the first fifteen trials performed twenty-four hours later. Improvement in second-day performance indicated successful long-term memory retention of the learned avoidance task. Behavioral data therefore allowed investigators to independently evaluate both acquisition of new information and subsequent retrieval of stored memory, two cognitive domains commonly impaired in Alzheimer’s disease [1].
Immediately after completion of behavioral testing, all animals were euthanized by decapitation, and several hormone-sensitive organs were carefully removed and weighed. Organs examined included the prostate gland, seminal vesicles, adrenal glands, thymus, and spleen. These measurements served as biological indicators of systemic estrogenic activity. Because 17β-estradiol possesses potent endocrine effects whereas 17α-estradiol exhibits much lower affinity for classical estrogen receptors, comparison of organ weights allowed investigators to determine whether cognitive improvements occurred in parallel with hormonal stimulation or independently of endocrine activity. Demonstrating preservation of peripheral organ weights despite improved learning would support the hypothesis that neuroprotective actions result primarily from antioxidant mechanisms rather than classical estrogen receptor activation [1].
The investigation consisted of four independent experiments, each including approximately thirty to thirty-six animals distributed among the treatment groups. Data from behavioral testing and organ weight measurements were expressed as mean values with corresponding measures of variability. Statistical analyses were performed using one-way analysis of variance (ANOVA), followed by Newman-Keuls multiple comparison testing to identify significant differences among experimental groups. This statistical approach enabled comparisons between healthy control animals, AF64A-treated rats receiving vehicle, and AF64A-treated animals receiving either dose of 17β-estradiol or 17α-estradiol. Through the integration of a validated Alzheimer’s disease model, controlled hormone administration, standardized behavioral testing, and physiological assessment of endocrine tissues, the investigators established a comprehensive experimental framework for determining whether 17α-estradiol could improve cognitive function while avoiding the undesirable hormonal effects associated with conventional estrogen therapy [1].
2) The study by Li and colleagues was designed to investigate whether stabilization of G-quadruplex (G4) structures within the GLI1 promoter could suppress gastric cancer progression and whether two FDA-approved compounds, alpha-estradiol (17α-estradiol) and (R)-(-)-ibuprofen, could be repurposed as G4-stabilizing agents. Because GLI1 is a major downstream transcription factor of the Hedgehog signaling pathway and is frequently overexpressed in gastric cancer, the investigators hypothesized that stabilizing a naturally occurring G4 structure within its promoter would inhibit GLI1 transcription, thereby suppressing tumor growth, invasion, metastasis, and stem cell-like behavior. To evaluate this hypothesis, the researchers integrated bioinformatic analyses, molecular biology techniques, biochemical assays, cultured gastric cancer cell experiments, xenograft mouse models, and mechanistic pathway studies to identify the molecular targets responsible for the observed anticancer effects [2].
The investigation began with an extensive analysis of publicly available cancer databases. Expression of GLI1 in gastric cancer was examined using the TIMER, GEPIA, and UALCAN databases to determine associations with tumor stage, lymph node involvement, and patient survival. The investigators also analyzed correlations between GLI1 and PRKACB, a downstream signaling molecule suspected to mediate GLI1 activity. Overall survival analyses were performed using The Human Protein Atlas, while correlation analyses between GLI1 and PRKACB expression were conducted using TIMER. These computational analyses established the clinical significance of both genes before laboratory experiments were initiated. To validate these observations experimentally, tissue microarrays containing paired gastric adenocarcinoma and adjacent normal tissues obtained from thirty patients were examined using immunohistochemistry to compare protein expression between malignant and nonmalignant tissues [2].
The in vitro studies utilized two human gastric cancer cell lines, AGS and HGC-27, together with the normal gastric epithelial cell line GES-1. Cells were maintained in standard culture media supplemented with fetal bovine serum and antibiotics under controlled incubation conditions. Experimental treatments included 1 μM alpha-estradiol, 1 μM (R)-(-)-ibuprofen, or 20 μM GANT61, a well-characterized GLI1 inhibitor that served as a positive control throughout the study. To investigate downstream signaling mechanisms, selected experiments also involved transfection of AGS and HGC-27 cells with PRKACB overexpression plasmids using Lipofectamine-mediated gene delivery. Successful transfection was verified by Western blot analysis before subsequent functional experiments were performed.
To determine whether the GLI1 promoter contained functional G-quadruplex structures capable of serving as therapeutic targets, the investigators first performed circular dichroism (CD) spectroscopy. Purified promoter sequences were analyzed under controlled experimental conditions to verify formation of characteristic G4 secondary structures. Following confirmation of G4 formation, the researchers generated both wild-type and mutant GLI1 promoter reporter constructs in which the predicted G-quadruplex-forming region had been disrupted. These constructs were introduced into gastric cancer cells, and dual-luciferase reporter assays were performed to evaluate promoter activity. An FDA-approved drug library was then screened using this reporter system to identify compounds that selectively suppressed activity of the wild-type promoter while producing little or no effect on the mutant construct. Candidate compounds identified during screening underwent additional validation using repeated luciferase assays and Western blot analysis to determine their ability to suppress GLI1 protein expression [2].
After identifying alpha-estradiol and (R)-(-)-ibuprofen as promising G4 stabilizers, the investigators evaluated their biological effects using several complementary in vitro functional assays. Cell proliferation was measured using EdU incorporation assays and colony formation assays, allowing assessment of DNA synthesis and long-term proliferative capacity. Cell migration was evaluated using wound-healing assays, in which standardized scratches were introduced into confluent cell monolayers and wound closure was monitored over twenty-four hours. Invasive behavior was examined using Transwell migration and invasion assays, with invasion chambers coated with Matrigel to simulate extracellular matrix barriers. To investigate cancer stem cell characteristics, researchers performed sphere formation assays, measuring the ability of single cells to generate spheroid colonies under low-adhesion conditions. Expression of stemness markers including CD44 and SOX2, as well as epithelial-mesenchymal transition (EMT) markers including Zeb1 and vimentin, was evaluated using Western blotting and immunohistochemistry.
The molecular mechanism linking GLI1 to PRKACB was investigated through several complementary experiments. Bioinformatic promoter analysis identified a putative GLI1 binding site within the PRKACB promoter. This prediction was tested using chromatin immunoprecipitation (ChIP) assays, in which DNA-protein complexes were cross-linked, immunoprecipitated using anti-GLI1 antibodies, and analyzed by quantitative PCR to determine whether GLI1 directly occupied the PRKACB promoter. Additional experiments evaluated how pharmacological inhibition of GLI1 or overexpression of PRKACB altered expression of downstream signaling proteins and epithelial-mesenchymal transition markers. Rescue experiments combining PRKACB overexpression with GLI1 inhibition helped determine whether PRKACB functioned as a critical downstream mediator of GLI1 signaling in gastric cancer cells [2].
To determine whether the in vitro findings translated to living organisms, the investigators conducted xenograft experiments using male BALB/c nude mice. Human HGC gastric cancer cells were implanted either subcutaneously to evaluate primary tumor growth or intravenously to establish experimental lung metastases. Mice were randomly assigned to treatment groups receiving alpha-estradiol, (R)-(-)-ibuprofen, GANT61, cisplatin, or combined cisplatin plus (R)-(-)-ibuprofen. Drugs were administered by daily intraperitoneal injection for one week. Tumor size was measured repeatedly throughout the study, and animals were euthanized after completion of treatment for collection of tumor tissues and lungs. Tumor weight, metastatic burden, and histological changes were assessed using hematoxylin and eosin staining together with immunohistochemical analysis of GLI1, PRKACB, Ki67, Zeb1, and vimentin expression. These experiments also evaluated whether (R)-(-)-ibuprofen enhanced the antitumor efficacy of cisplatin chemotherapy [2].

Discussion
1) The study conducted by Lermontova et al demonstrated that both 17β-ED and 17α-ED significantly improved learning and memory in rats with chronic cholinergic deficiency induced by the selective neurotoxin AF64A. Most importantly, the investigators showed for the first time that 17α-estradiol, an estrogen isomer with minimal classical hormonal activity, effectively reversed cognitive deficits produced by chronic cholinergic degeneration. Although both estrogens enhanced cognitive performance, 17α-estradiol produced greater improvements while causing substantially fewer effects on hormone-sensitive peripheral tissues. These findings suggested that the neuroprotective actions of estradiols are primarily mediated through antioxidant and neuroprotective mechanisms rather than through activation of classical estrogen receptors, making 17α-estradiol a potentially safer therapeutic candidate for treating cognitive impairment associated with neurodegenerative diseases such as Alzheimer’s disease [1].
Before evaluating the effects of estrogen treatment, the investigators first confirmed that surgical castration itself did not alter the animals’ response to AF64A. Previous work from the research group had demonstrated that castrated rats exhibited behavioral responses to AF64A comparable to those of intact animals, indicating that removal of endogenous sex hormones did not influence susceptibility to cholinergic injury. Following intracerebroventricular administration of AF64A, rats displayed marked impairments in both learning acquisition and memory retrieval during the active avoidance task. Compared with control animals receiving artificial cerebrospinal fluid alone, AF64A-treated rats showed a substantial reduction in the percentage of correct conditioned avoidance responses during both the initial learning session and the memory retention test performed twenty-four hours later. On the first day of testing, control animals achieved approximately 91% correct avoidance responses, whereas AF64A-treated rats achieved only about 52%. During the second-day memory test, control animals maintained approximately 86% correct responses, while AF64A-treated animals declined further to only 42%. These findings confirmed that chronic cholinergic deficiency produced profound deficits in both acquisition of new information and long-term memory retrieval, successfully reproducing cognitive impairments characteristic of Alzheimer’s disease [1].
The effects of 17α-estradiol proved particularly noteworthy because this compound demonstrated greater cognitive efficacy than 17β-estradiol despite possessing much weaker estrogenic activity. Unlike 17β-estradiol, both tested doses of 17α-estradiol significantly improved learning and memory performance. Animals receiving the higher 40 μg/kg dose showed approximately 77% correct avoidance responses during the learning session and approximately 63% during memory retrieval, representing substantial improvement over untreated AF64A animals. Even more strikingly, rats treated with only 4 μg/kg of 17α-estradiol achieved approximately 74% correct responses during learning and nearly 83% correct responses during the second-day memory test. Thus, the lower dose of 17α-estradiol produced memory retrieval performance nearly equivalent to that observed in healthy control animals and comparable to the higher dose of 17β-estradiol. These findings demonstrated that 17α-estradiol was a more potent enhancer of cognitive function than 17β-estradiol in this experimental model despite its much weaker interaction with classical estrogen receptors.
17α-estradiol produced minimal endocrine effects despite its strong cognitive benefits. Neither the low nor high dose significantly altered the weights of the prostate gland or seminal vesicles, indicating little activation of classical estrogen-responsive reproductive tissues. The lower 4 μg/kg dose produced virtually no measurable changes in any hormone-sensitive organ examined. Only the higher 40 μg/kg dose modestly increased adrenal gland weight and slightly reduced thymus weight, effects that were considerably smaller than those produced by 17β-estradiol. This dissociation between cognitive improvement and endocrine stimulation was one of the study’s most important findings because it demonstrated that significant enhancement of learning and memory could be achieved without producing the widespread hormonal effects associated with conventional estrogen therapy. These observations suggested that the mechanisms responsible for neuroprotection differ substantially from those mediating peripheral endocrine responses [1].
Based on these findings, the investigators proposed that the cognitive benefits of both estradiols are unlikely to result primarily from activation of classical nuclear estrogen receptors. They noted that estrogen receptor density is relatively low within important cognitive structures such as the hippocampus and cerebral cortex and emphasized that 17α-estradiol possesses much lower affinity for these receptors than 17β-estradiol. Despite this reduced receptor affinity, 17α-estradiol produced greater improvements in learning and memory than the hormonally active isomer. The authors therefore argued that alternative mechanisms must account for the observed neuroprotective effects. They suggested that enhancement of neuronal resistance to AF64A-induced injury, stimulation of compensatory regenerative processes, and direct antioxidant actions represented more plausible explanations for the improvements in cognitive performance. Previous studies had demonstrated that oxidative stress accompanies AF64A-induced cholinergic degeneration as well as Alzheimer’s disease pathology, making antioxidant protection a biologically plausible mechanism.
The investigators concluded that the superior cognitive efficacy of 17α-estradiol, combined with its minimal endocrine activity, strongly supports the hypothesis that antioxidant properties rather than hormonal effects underlie the beneficial actions of estradiols on cognition. They noted that previous experimental work had demonstrated that 17α-estradiol is a more potent antioxidant than 17β-estradiol, a finding consistent with the greater cognitive improvement observed at substantially lower doses. Because oxidative stress is a major contributor to neuronal degeneration in Alzheimer’s disease, the authors proposed that the antioxidant capacity of 17α-estradiol protects vulnerable cholinergic neurons from damage while promoting functional recovery of learning and memory. Overall, the study provided the first direct evidence that 17α-estradiol can effectively compensate for cognitive impairment caused by chronic cholinergic dysfunction while avoiding the pronounced hormonal side effects associated with conventional estrogen therapy. These findings identified 17α-estradiol as a promising neuroprotective compound for future investigation in age-related cognitive decline and neurodegenerative disorders [1].
2) The study conducted by researchers Li et al demonstrated that alpha-estradiol and (R)-(-)-ibuprofen effectively inhibited gastric cancer progression by stabilizing a G4 structure within the GLI1 promoter, thereby suppressing GLI1 transcription and its downstream signaling pathway. Through a combination of bioinformatic analyses, in vitro functional assays, mechanistic studies, and mouse xenograft models, the investigators showed that both compounds significantly reduced gastric cancer cell proliferation, migration, invasion, stem cell-like properties, tumor growth, and metastasis. Furthermore, the study identified PRKACB as a previously unrecognized downstream target directly regulated by GLI1 and demonstrated that inhibition of the GLI1/PRKACB signaling axis accounted for much of the observed antitumor activity. Overall, the findings provided strong evidence that pharmacological stabilization of promoter G-quadruplexes represents a novel therapeutic strategy for targeting GLI1-driven gastric cancer [2].
The investigators first established the clinical relevance of GLI1 in gastric cancer. Analysis of multiple publicly available cancer databases revealed that GLI1 expression was significantly elevated in gastric tumors compared with normal gastric tissues. Increased GLI1 expression correlated closely with more advanced clinical stage, greater lymph node involvement, and poorer overall survival among patients with gastric cancer. Immunohistochemical analysis of tissue microarrays confirmed these findings, demonstrating substantially stronger GLI1 protein staining in gastric carcinoma specimens than in adjacent noncancerous tissues. Together, these observations confirmed that GLI1 is closely associated with gastric cancer progression and poor clinical outcome, providing strong justification for targeting GLI1 therapeutically.
The next series of experiments confirmed that the GLI1 promoter contains a functional G-quadruplex structure that can be pharmacologically targeted. Circular dichroism spectroscopy demonstrated characteristic spectral patterns consistent with stable G4 formation. Mutation of the predicted G-quadruplex sequence disrupted this structure and significantly altered promoter activity in luciferase reporter assays. Screening of an FDA-approved drug library identified six compounds capable of selectively affecting the wild-type promoter while producing minimal effects on the mutated promoter. Among these candidates, alpha-estradiol and (R)-(-)-ibuprofen emerged as the most effective G4 stabilizers. Dual-luciferase assays demonstrated that both compounds significantly reduced GLI1 promoter activity, and subsequent Western blot analyses confirmed corresponding reductions in GLI1 protein expression in both AGS and HGC gastric cancer cell lines. These experiments established that both drugs suppress GLI1 expression through stabilization of the promoter G-quadruplex rather than through nonspecific inhibition of gene expression [2].
Functional studies demonstrated that suppression of GLI1 translated into substantial inhibition of malignant cellular behavior. Colony formation assays showed that treatment with either alpha-estradiol or (R)-(-)-ibuprofen significantly reduced the number and size of colonies formed by gastric cancer cells, indicating impaired long-term proliferative capacity. Similar findings were observed in EdU incorporation assays, where treated cells exhibited reduced DNA synthesis and fewer proliferating cells compared with untreated controls. Collectively, these results demonstrated that stabilization of the GLI1 G-quadruplex effectively suppressed gastric cancer cell proliferation and limited the capacity of tumor cells to expand in culture.
Both compounds also produced pronounced inhibitory effects on tumor cell migration and invasion. In wound-healing assays, closure of the experimental wound occurred much more slowly in alpha-estradiol- and ibuprofen-treated cultures than in untreated controls, indicating significantly impaired migratory capacity. Transwell migration and Matrigel invasion assays further confirmed these observations, showing marked reductions in the number of cells capable of migrating through porous membranes or invading through extracellular matrix barriers following treatment with either compound. These functional improvements were accompanied by decreased expression of the EMT markers Zeb1 and vimentin, suggesting that suppression of EMT contributed directly to the reduced invasive phenotype. These findings demonstrated that stabilization of the GLI1 promoter G-quadruplex not only inhibited tumor cell growth but also substantially reduced the metastatic potential of gastric cancer cells.
The in vivo xenograft experiments strongly supported the in vitro findings. Nude mice implanted with HGC gastric cancer cells and treated with alpha-estradiol or (R)-(-)-ibuprofen developed significantly smaller tumors than untreated control animals. Measurements obtained throughout the experiment showed substantially slower tumor growth, reduced final tumor volumes, and markedly lower tumor weights in both treatment groups. The degree of tumor inhibition was comparable to that produced by GANT61, a well-established experimental GLI1 inhibitor, indicating that both FDA-approved compounds effectively suppressed GLI1-driven tumor growth in living animals. Tail vein metastasis experiments further demonstrated that treated mice developed significantly fewer pulmonary metastatic lesions than untreated controls. Histological examination confirmed reduced metastatic burden within the lungs, while immunohistochemical staining showed decreased expression of GLI1, Zeb1, and vimentin within tumor tissues. These findings established that alpha-estradiol and (R)-(-)-ibuprofen inhibit both primary tumor growth and metastatic dissemination in vivo [2].
An additional clinically relevant finding involved the combination of (R)-(-)-ibuprofen with cisplatin chemotherapy. Mice receiving combination treatment developed substantially smaller tumors than animals treated with cisplatin alone. Tumor weights were significantly reduced, and immunohistochemical analyses demonstrated further decreases in Ki67, Zeb1, and vimentin expression compared with chemotherapy alone. Because Ki67 is a marker of cellular proliferation and Zeb1 and vimentin are key regulators of epithelial-mesenchymal transition, these findings suggest that (R)-(-)-ibuprofen enhances the antitumor efficacy of conventional chemotherapy while simultaneously suppressing metastatic behavior. The authors proposed that G4-stabilizing compounds could therefore serve as useful adjunctive agents alongside established cytotoxic therapies.
Mechanistic investigations identified PRKACB as a critical downstream mediator of GLI1 signaling. Database analyses demonstrated a strong positive correlation between GLI1 and PRKACB expression in gastric cancer, with PRKACB overexpression also predicting poorer patient survival. Both proteins were highly expressed in gastric tumor specimens but were substantially reduced following treatment with alpha-estradiol or (R)-(-)-ibuprofen. Chromatin immunoprecipitation experiments confirmed that GLI1 directly binds to the PRKACB promoter, demonstrating that PRKACB is a direct transcriptional target of GLI1. Pharmacological inhibition of GLI1 using GANT61 reduced PRKACB expression, whereas overexpression of PRKACB partially restored expression of EMT markers despite GLI1 inhibition. Rescue experiments further showed that PRKACB overexpression reversed many of the inhibitory effects of GLI1 blockade on proliferation, migration, invasion, and epithelial-mesenchymal transition, confirming that PRKACB functions as an essential downstream effector of GLI1 signaling in gastric cancer cells [2].
The final series of experiments demonstrated that the GLI1/PRKACB pathway also regulates gastric cancer stem cell-like properties. Inhibition of GLI1 significantly reduced expression of the stem cell markers CD44 and SOX2 in both AGS and HGC cell lines. Sphere formation assays showed marked reductions in the number and size of tumor spheroids following GLI1 inhibition, indicating impaired self-renewal capacity. Although PRKACB overexpression partially restored sphere formation and stem cell marker expression, these effects remained significantly attenuated when GLI1 activity was inhibited, demonstrating that suppression of GLI1 signaling effectively diminishes cancer stemness. Immunohistochemical analysis of patient tissue microarrays further confirmed a strong positive correlation between GLI1 and PRKACB protein expression in clinical gastric cancer specimens. Collectively, the investigators concluded that alpha-estradiol and (R)-(-)-ibuprofen inhibit gastric cancer progression by stabilizing G-quadruplex structures within the GLI1 promoter, thereby suppressing GLI1 transcription, downregulating PRKACB signaling, reducing epithelial-mesenchymal transition and cancer stemness, and ultimately limiting tumor growth and metastasis [2].

Disclaimer

**LAB USE ONLY**
*This information is for educational purposes only and does not constitute medical advice. THE PRODUCTS DESCRIBED HEREIN ARE FOR RESEARCH USE ONLY. All clinical research must be conducted with oversight from the appropriate Institutional Review Board (IRB). All preclinical research must be conducted with oversight from the appropriate Institutional Animal Care and Use Committee (IACUC) following the guidelines of the Animal Welfare Act (AWA).

Citations

[1] Lermontova, N.N., P’chev, V.K., Beznosko, B.K. et al. Effects of 17β-estradiol and its isomer 17α-estradiol on learning in rats with chronic cholinergic deficiency in the brain. Bull Exp Biol Med 129, 442–444 (2000). https://doi.org/10.1007/BF02439796

[2] Li Q, Pan P, Xian Q, et al. Alpha-estradiol and (R)-(-)-ibuprofen inhibit gastric cancer progression via GLI1 G-quadruplex. Front Pharmacol. 2025;16:1492694. Published 2025 Apr 4. doi:10.3389/fphar.2025.1492694

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