Main Research Findings

1) In an animal model of optic nerve injury, Compound 7p was shown to promote neuronal outgrowth and regeneration.

2) In an animal model of Alzheimer’s disease, Compound 7p was found to reduce cognitive and memory deficits by inhibiting butyrylcholinesterase.

 

Selected Data
1) The study by Ku et al investigated the ability of small-molecule compounds to stimulate neuronal outgrowth and ultimately promote axon regeneration. The researchers used a phenotypic, cell-based screening strategy designed to identify compounds capable of activating cellular mechanisms associated with neurite extension. The compounds utilized in the study were initially evaluated at 10 μM using P19 embryonic carcinoma cells that had been transiently transfected with a NeuroD2 expression construct. NeuroD2 was used to induce neuronal differentiation, causing the P19 cells to develop neurite-like extensions that could be visualized and quantified. Compounds producing more than a twofold increase in neurite outgrowth compared with the DMSO-treated control were selected for further investigation. This primary screen produced 185 confirmed active compounds, corresponding to a 0.11% hit rate [1].
The compounds identified in the initial screen were subsequently evaluated using primary rat hippocampal neurons to determine whether their activity translated from the P19 model into a more physiologically relevant neuronal system. Primary hippocampal and cortical neurons were obtained from embryonic day 18 Sprague–Dawley rats. The hippocampus and cerebral cortex were separately dissected, mechanically dissociated, washed, filtered, and plated. Following a 24-hour incubation period, the cells were exposed to test compounds for 48 hours before neuronal morphology was evaluated. Neuronal structures were visualized using indirect immunofluorescence against βIII-tubulin, a neuronal marker. Fluorescence images were collected from four fields per well using a high-content screening system, and neurite morphology was quantified using neuronal profiling software. This secondary screening process identified a group of compounds sharing a sulfonamidoacetamide structural scaffold. Compound 1 was selected as the most promising member of this group because it produced substantial neurite elongation in primary hippocampal neurons and demonstrated comparable activity in primary cortical neurons. However, Compound 1 displayed poor water solubility and extremely limited metabolic stability, making it unsuitable for direct in vivo evaluation. Consequently, the researchers initiated structure–activity-guided chemical optimization using neurite outgrowth in primary cortical neurons as the principal biological readout [1].
Following identification of Compound 7p as a particularly promising analogue, the researchers examined its activity in retinal neurons. Retinal ganglion cells were isolated from postnatal day 7 Sprague–Dawley rats using a commercial RGC isolation kit. Cells were plated on poly-D-lysine- and laminin-coated coverslips at 200,000 cells per well and treated with Compound 7p at 0, 2, 10, or 20 μM. After 72 hours, the cells were fixed and stained with the SMI-312 anti-neurofilament antibody to visualize axons. Retinal neuronal growth was quantified by categorizing cells according to axonal length: less than 50 μm, 50–100 μm, 100–200 μm, or greater than 200 μm. Cell size and morphology were used to identify retinal ganglion cells, with cells having a soma diameter greater than 10 μm selected for analysis. Cell viability was also assessed by counting cells in nine consecutive nonoverlapping microscopic fields.
The final experimental stage evaluated Compound 7p in vivo using an optic nerve crush model. Male Sprague–Dawley rats approximately eight weeks old and weighing 200–250 g were housed under controlled temperature, humidity, and 12-hour light/dark conditions. Animals were randomly assigned to a sham-operated control group or an optic nerve crush group treated with Compound 7p. Under anesthesia, the retrobulbar optic nerve was exposed and crushed with forceps for 15 seconds approximately 2 mm behind the optic head. The experimental animals subsequently received intravitreal injections of Compound 7p at 0.22 μg in 5 μL per eye once every four days for three weeks, while the sham-operated animals received saline. Following the treatment period, the eyes and optic nerves were collected, fixed in paraformaldehyde, cryoprotected, embedded, sectioned, and immunostained. GAP-43 was used as a marker of growing axons, and ImageJ was employed to quantify GAP-43-positive axons at 0.5, 1.0, and 1.5 mm from the optic nerve crush site [1].
2) The research team of Yu et al. conducted a comprehensive investigation of a series of pyranone-carbamate derivatives designed to provide both butyrylcholinesterase (BuChE) inhibition and anti-neuroinflammatory effects. A total of 19 new compounds, labeled 7a–7s, were synthesized using a 3-hydroxylpyranone core linked to an aromatic carbamate moiety through a styrene-based connecting group. The overall design was motivated by the potential benefit of simultaneously enhancing cholinergic neurotransmission through BuChE inhibition and limiting neuroinflammation, which represents another important pathological component of Alzheimer’s disease. The researchers had previously identified the 3-hydroxylpyranone structure as a promising scaffold because of its reported anti-Alzheimer’s, anti-inflammatory, antioxidant, neuroprotective, and brain-penetrating properties. A carbamate functionality was incorporated because of its established ability to interact with cholinesterase enzymes, while the styrene group functioned as a structural linker between the pyranone and carbamate regions. Following synthesis, the compounds underwent a series of chemical, enzymatic, cellular, computational, permeability, safety, and behavioral assessments to determine their biological properties and identify the most promising candidate [2].
The structures and purity of the synthesized derivatives were verified using several analytical techniques. Proton (^1H) and carbon (^13C) nuclear magnetic resonance spectroscopy were used to characterize the molecular structures, while high-resolution mass spectrometry (HRMS) provided information supporting the expected molecular masses. Melting-point measurements and high-performance liquid chromatography (HPLC) were also performed to evaluate the physical characteristics and purity of the synthesized compounds. All compounds selected for biological evaluation demonstrated purities exceeding 95%. Compound 7p underwent additional structural analysis using X-ray crystallography, which provided direct confirmation of its molecular structure and established the trans configuration of the vinyl group formed during the Heck coupling reaction. Thin-layer chromatography was used throughout the synthetic procedures to monitor reaction progress. Collectively, these analytical methods provided structural confirmation and ensured that the compounds subjected to biological testing were adequately characterized and sufficiently pure.
The researchers initially assessed the compounds for their ability to inhibit acetylcholinesterase (AChE) and BuChE using a modified Ellman colorimetric assay. Three enzyme preparations were examined: electric-eel acetylcholinesterase (eeAChE), equine-serum butyrylcholinesterase (eqBuChE), and human-serum butyrylcholinesterase (huBuChE). Tacrine was included as the reference cholinesterase inhibitor. During the initial screening phase, the compounds were evaluated at 20 μM against eeAChE and 10 μM against BuChE. Molecules that produced greater than 50% enzyme inhibition were subsequently subjected to concentration-response experiments to determine their half-maximal inhibitory concentrations (IC₅₀). Each enzymatic reaction contained a 100 μL final volume consisting of the test compound, DTNB, enzyme, and phosphate-buffered saline maintained at pH 8.0.
Following incubation at 37°C, the appropriate substrate, either acetylthiocholine or butyrylthiocholine, was added. Enzymatic activity was monitored by measuring absorbance at 412 nm, and the resulting data were used to calculate IC₅₀ values. Compound 7p was subsequently subjected to more detailed kinetic experiments in which multiple concentrations of both inhibitor and butyrylthiocholine were examined. Absorbance measurements were collected at one-minute intervals over a 10-minute period. Dixon and Cornish-Bowden plots were then generated through linear regression to determine the type of inhibition produced by 7p and calculate its corresponding inhibition constants [2].
The anti-neuroinflammatory properties of the synthesized compounds were examined using BV-2 mouse microglial cells and an inflammatory model based on lipopolysaccharide (LPS)-stimulated nitric oxide production. Before evaluating inflammatory activity, the researchers performed an MTT viability assay to establish whether the compounds affected cellular survival at the concentrations intended for testing. This preliminary step helped ensure that reductions in nitric oxide production would reflect anti-inflammatory activity rather than nonspecific cellular toxicity. BV-2 cells were seeded at a density of 1 × 10^4 cells per well and treated with the compounds for 24 hours before exposure to MTT. After incubation, the resulting formazan product was dissolved in dimethyl sulfoxide (DMSO), and absorbance was measured at 490 nm. Since treatment at 10 μM did not produce significant differences in cell viability for the tested compounds or hydrocortisone, this concentration was selected for the subsequent inflammation experiments. For the nitric oxide assay, BV-2 cells were seeded at 5 × 10^4 cells per well and allowed to incubate for 24 hours. The test compounds were then introduced for one hour before stimulation with LPS at a final concentration of 1 μg/mL. After an additional 24-hour incubation period, culture supernatants were collected and analyzed for nitric oxide production using a commercial assay based on the Griess reaction. Hydrocortisone was used as the reference compound for evaluating anti-inflammatory activity [2].
Because Alzheimer’s disease involves pathology within the central nervous system, the investigators also examined whether the compounds possessed physicochemical and permeability characteristics compatible with central nervous system drug development. SwissADME was first employed to estimate the physicochemical characteristics, drug-likeness, and predicted blood-brain barrier (BBB) permeability of compounds 7a–7s. Compound 7p, which emerged as a particularly promising candidate from the biochemical and cellular studies, was subsequently examined experimentally using a parallel artificial membrane permeation assay designed to approximate BBB penetration. Compound 7p and selected reference drugs were initially dissolved in DMSO and diluted with phosphate-buffered saline. The solutions were introduced into a donor compartment containing a membrane formulated with porcine brain lipids, while the acceptor compartment contained PBS. The donor and acceptor plates were assembled and maintained at 25°C for 10 hours. Following incubation, the amount of compound that had passed through the membrane into the acceptor compartment was quantified spectrophotometrically. These measurements were used to calculate the apparent permeability coefficient (Pe). Six commercially available drugs with established BBB permeability characteristics were included as reference compounds to validate the performance and reliability of the PAMPA-BBB system.
The researchers then investigated the acute safety profile of Compound 7p in mice. Sixteen ICR mice, with equal representation of males and females, were randomly divided into a control group and a treatment group. Control animals received 0.5% carboxymethyl cellulose sodium (CMC-Na), whereas the experimental animals received a single oral dose of 7p at 1000 mg/kg. The animals were monitored for 14 days following administration, with observations focused on mortality, behavioral abnormalities, food and water consumption, and changes in body weight. At the conclusion of the observation period, the animals were euthanized and major organs, including the heart, liver, spleen, and brain, were collected for histopathological examination. Tissue sections were stained with hematoxylin and eosin and examined for evidence of structural abnormalities or pathological changes [2].
Finally, the investigators evaluated the effects of Compound 7p on cognitive performance using a scopolamine-induced mouse model of cognitive impairment. C57BL/6J mice were divided into five experimental groups, consisting of a control group, scopolamine-treated group, rivastigmine-treated group, and two groups receiving different doses of Compound 7p. Each group contained eight animals. Scopolamine was administered intraperitoneally at 5 mg/kg from days 1 through 26 to induce cognitive deficits. Beginning on day 11, the treatment groups received either rivastigmine at 1 mg/kg or Compound 7p at doses of 1 or 5 mg/kg by oral administration once daily. Cognitive performance was evaluated between days 21 and 26 using the Morris water maze. During the acquisition phase, the mice completed five days of training in which they were required to locate a submerged platform. A probe trial was subsequently conducted with the platform removed, allowing the investigators to evaluate spatial memory based on the animals’ search behavior and the number of times they crossed the previous platform location. Swimming trajectories were continuously recorded using a camera and subsequently analyzed to quantify behavioral performance. Through this sequential experimental design, the study evaluated Compound 7p from initial chemical synthesis and enzyme inhibition through cellular anti-inflammatory activity, BBB permeability, acute toxicity, and ultimately cognitive performance in an animal model of memory impairment [2].

 

Discussion
1) The results of the study performed by Ku et al demonstrated that the screening and optimization strategy successfully identified that Compound 7p had the ability to stimulate neuronal outgrowth and promote axonal regeneration in an experimental model. The initial phenotypic screen evaluated approximately 170,000 synthetic compounds for their capacity to increase neurite extension in NeuroD2-transfected P19 cells. Compounds were tested at 10 μM, and those producing more than a twofold increase in neurite outgrowth compared with DMSO controls were selected. Of the compounds screened, 185 were confirmed as active, corresponding to a relatively low hit rate of 0.11%. Secondary testing in primary rat hippocampal neurons narrowed the candidates further and revealed a group of chemically related compounds containing a sulfonamidoacetamide core. Among these compounds, Compound 1 displayed the strongest initial activity. Its neurite-elongating effects reached a plateau between 10 and 20 μM, where outgrowth was approximately threefold greater than the control, while activity was lost at concentrations below 1 μM. Compound 1 also increased neurite elongation in primary cortical neurons. These findings established the sulfonamidoacetamide scaffold as a promising starting point for further optimization [1].
Despite its biological activity, Compound 1 had unfavorable physicochemical characteristics that limited its usefulness as an in vivo candidate. Structure–activity-guided optimization was therefore undertaken to identify analogues with improved activity and pharmacological properties. Modification of the C-ring substituents revealed that the position and chemical characteristics of the substituent influenced neurite outgrowth. Compound 1 produced a 3.2-fold increase in neurite outgrowth at 10 μM, while the 3-ethoxy derivative 7b produced a 1.8-fold increase and the unsubstituted derivative 7c produced a 2.0-fold increase. Other substitutions, including 2-ethyl, 2-fluoro, and 2-bromo groups, produced lower or intermediate activity. Some structural replacements, particularly imidazole- and thiazole-containing derivatives, produced cytotoxicity in the primary cortical neuron assay. These results indicated that relatively specific structural characteristics were required to preserve biological activity [1].
Compound 7p was shown to emerge as the most potent pyridine-containing analogue. Importantly, Compound 7p had a calculated log P of 2.43, substantially lower than the log P of 3.76 measured for Compound 1. This reduction in lipophilicity was accompanied by a major improvement in metabolic stability: 61.2% of Compound 7p remained following the S9 incubation compared with only 0.7% of Compound 1. Thus, Compound 7p combined strong neurite outgrowth activity with substantially improved metabolic stability, making it the preferred derivative for subsequent biological evaluation.
The researchers next determined whether the effects observed in cultured neurons could extend to axonal growth in retinal neurons. Compound 7p was tested at concentrations ranging from 2 to 20 μM for 72 hours. Retinal neuronal cells were stained with an anti-neurofilament antibody to identify axonal structures, and axons were categorized according to their lengths. The study reported that Compound 7p stimulated axonal growth across the different length categories, with the strongest effect observed at 10 μM. The viability analysis did not show a significant reduction in the number of live retinal neuronal cells following Compound 7p treatment, thus, the increase in axonal extension was not simply attributable to selective survival of a small neuronal population. Treatment with 2–20 μM Compound 7p did not produce a significant difference in total numbers of live cells, while immunofluorescence analysis demonstrated increased axonal growth. The retinal experiments therefore provided evidence that the compound’s effects were associated with axonal extension rather than an obvious cytotoxic effect [1].
The most important result was obtained from the optic nerve crush model. Rats with crushed optic nerves received intravitreal Compound 7p at 0.22 μg per eye once every four days for three weeks. Following treatment, optic nerve sections were stained for GAP-43, a marker associated with growing axons. Compared with PBS-treated injured controls, Compound 7p-treated animals demonstrated substantially greater extension of GAP-43-positive axons beyond the injury site. Increased numbers of GAP-43-positive axons were observed at 500, 1,000, and 1,500 μm distal to the crush center. The difference was statistically significant at the 1,500 μm measurement point, where the injured control group had approximately 0.22 ± 0.081 GAP-43-positive axons compared with 0.70 ± 0.20 in the Compound 7p-treated group. The authors therefore concluded that the neurite outgrowth activity observed in cultured neurons translated into enhanced axon regeneration in vivo [1].

 

Figure 1: Changes in axonal regeneration in the optic nerve crush site following treatment with Compound 7p.
Overall, the study established Compound 7p as the most favorable derivative produced through the investigators’ phenotypic screening and structure–activity optimization program. Its activity was demonstrated in multiple neuronal systems, including primary hippocampal, cortical, and retinal neurons, and its improved metabolic stability distinguished it from the original Compound 1. Compound 7p increased the growth of GAP-43-positive axons following optic nerve injury, providing experimental evidence that the compound could promote regeneration within an injured central nervous system pathway. However, the researchers emphasized that the mechanism responsible for Compound 7p-induced axon regeneration in vivo remained unresolved. The study did not establish a specific molecular target or demonstrate improvements in functional neurological behavior or cognition. Consequently, the findings support Compound 7p primarily as an experimental axon-regeneration and neuroregenerative compound, rather than establishing it as a clinically validated nootropic [1].
2) The research team of Yu et al. synthesized 19 pyranone-carbamate derivatives (7a–7s) and identified Compound 7p as the strongest overall candidate based on its BuChE inhibition and anti-neuroinflammatory activity. Structural analyses confirmed the synthesized compounds, with all biologically tested compounds showing greater than 95% purity. X-ray crystallography further confirmed the structure and trans configuration of 7p.Structure–activity relationship analysis showed that modifications to the pyranone and linker regions significantly affected BuChE inhibition. Compound 7l, which lacked the 6-methyl group, inhibited eqBuChE and huBuChE with IC₅₀ values of 8.10 and 6.93 nM, respectively. Compound 7m, containing a hydroxymethyl group, produced values of 5.22 and 16.53 nM. Larger substituents in 7n and 7o reduced activity, whereas replacing the O-benzyl group with the smaller O-methyl group produced 7p. Compound 7p demonstrated the strongest BuChE inhibition, with IC₅₀ values of 4.68 ± 1.39 nM for eqBuChE and 9.12 ± 0.57 nM for huBuChE [2].
The compounds also reduced LPS-induced nitric oxide production in BV-2 microglial cells. Compound 7k produced the greatest inhibition at 35.41% at 10 μM, although its BuChE activity was comparatively weak. Compound 7p reduced NO production by 28.82%, an effect comparable to hydrocortisone. Therefore, 7p provided the best overall balance between BuChE inhibition and anti-inflammatory activity. Structural analysis suggested that modifications such as replacing the 6-methyl group with hydroxymethyl, changing O-benzyl to O-methyl, and altering the vinyl linker influenced anti-inflammatory activity.
Kinetic experiments demonstrated that 7p acted as a mixed-type BuChE inhibitor. The inhibition constants were 3.15 nM for the free enzyme and 3.84 nM for the enzyme-substrate complex. Molecular docking supported these findings, showing interactions between the carbamate group and catalytic residues Ser-198 and His-438, along with additional interactions involving Asp-70 and Thr-120. Docking with AChE suggested that its narrower active-site gorge limited access of 7p to the catalytic region, providing a possible explanation for the compound’s selectivity toward BuChE [2].
SwissADME analysis indicated favorable drug-like properties for the compounds. Experimental PAMPA-BBB testing showed that 7p had a permeability coefficient of 5.70 × 10⁻⁶ cm/s, placing it in the study’s high-BBB-permeability category. Acute toxicity testing also produced favorable results. Mice receiving 1000 mg/kg of 7p showed no deaths or obvious behavioral abnormalities during 14 days of observation. Body weight generally increased, and histological examination of the heart, liver, spleen, and brain revealed no obvious pathological abnormalities. The reported acute oral LD₅₀ was therefore greater than 1000 mg/kg under the tested conditions [2].

 

Figure 2: Changes in body weight of animals treated with Compound 7p.
Compound 7p also improved cognitive performance in scopolamine-treated mice. Scopolamine increased escape latency to 52.63 seconds compared with 20.82 seconds in controls and reduced platform crossings to 1.5 versus 3.4 in controls. Rivastigmine reduced latency to 31.15 seconds and increased crossings to 3.0. Treatment with 7p reduced escape latency to 30.24 seconds at 1 mg/kg and 29.12 seconds at 5 mg/kg, while platform crossings increased to 3.3 and 3.5, respectively. These results indicated that 7p improved scopolamine-induced deficits in spatial learning and memory, with effects comparable to rivastigmine.
Overall, Compound 7p emerged as the leading molecule because it combined potent and selective BuChE inhibition, anti-neuroinflammatory activity, favorable drug-like characteristics, high BBB permeability, encouraging acute tolerability, and cognitive benefits in a mouse model. These findings support further investigation of 7p as a potential Alzheimer’s disease lead compound, although additional pharmacokinetic, long-term safety, efficacy, and clinical studies are required [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] Ku JM, Park K, Lee JH, et al. Discovery, Optimization, and Biological Evaluation of Sulfonamidoacetamides as an Inducer of Axon Regeneration. J Med Chem. 2016;59(10):4676-4687. doi:10.1021/acs.jmedchem.6b00015

[2] Yu C, Liu X, Ma B, et al. Novel anti-neuroinflammatory pyranone-carbamate derivatives as selective butyrylcholinesterase inhibitors for treating Alzheimer’s disease. J Enzyme Inhib Med Chem. 2024;39(1):2313682. doi:10.1080/14756366.2024.2313682

 

Compound 7P and Axonal Regeneration

Compound 7P is a nootropic compound originally developed to assist in neurite outgrowth and cognitive enhancement. Compound 7P is currently being researched to determine the role it could potentially play in terms of axon regeneration. Degeneration of axons can occur for a number of reasons, most common being trauma or injury, neurological diseases, and aging. Unfortunately, once the neurons are damaged they cannot repair themselves or regenerate without additional assistance.

Some of the most common methods of growth promotion focus on understanding the specific mechanisms of action and the manipulation of various signaling pathways. The most prevalent mechanisms typically involve epigenetic regulation of gene transcription, development-dependent transcription, and the mTOR and STAT3 signaling pathways. Researchers Park et. Al have discovered that altering the expression of these pathways can effectively lead to axon regeneration in the CNS.

Building off the work of Park et. Al, Ku et. Al have attempted to find additional modalities that will result in axon growth. The research team was able to visually assess and measure all in vitro neurite outgrowth through the use of phenotypic cell-based screens. It’s important to note that using these phenotypic small screen methods of measurement allow researchers to identify different types of protein targets and explain the mechanisms of various signaling pathways. Furthermore, being able to track axon elongation via phenotypic small screen provides an opportunity to more accurately pharmacologically manipulate the different factors assisting axon regeneration.

 

Use of Compound 7P to Promote Optic Nerve Regeneration

The research team of Ku et. Al was able to use phenotypic screening in order to identify compound 7P. They concluded that compound 7P was able to improve neurite outgrowth in the primary neurons of the hippocampus, cerebral cortex, and retina. Further testing found that in animal models, compound 7P was able to induce regeneration of the optic nerves in cases of injury.

The study initially began with treating retina neuronal cells with doses of either 2 or 20 μM of compound 7P. The cells were then incubated for 72 hours and treated with paraformaldehyde and an anti-neurofilament antibody in order to identify and measure axonal changes. During observation of the cultures the researchers were able to measure cell body size and morphology in order to identify retinal ganglion cells (RGCs). That being said, results of this initial study found that compound 7P led to significant axon growth. Axonal growth increased the most when the cells were treated with a 10 μM dose of the compound.

The second portion of the study was to determine if treatment with compound 7P would elicit the same effect in the RGCs of injured optic nerves as it did in healthy RGCs. The crushed optic nerves were treated with either a placebo, or a daily dose of 0.22 μg per eye, for 3 weeks. Following treatment, the animals were euthanized and cross sections of the optic nerves were stained with an anti-GAP43 antibody so researchers could efficiently identify and measure axonal growth. Results found that when the crushed optic nerves were treated with compound 7P the axons grew remarkably farther past the lesion epicenter than the nerves treated with a placebo. The results of this study suggest that further research should be conducted in order to determine how compound 7P can potentially increase axon growth and treat neuronal damage throughout the central nervous system (https://pubs.acs.org/doi/10.1021/acs.jmedchem.6b00015#).

 

Effects of Compound 7P Against Cervical Cancer

In addition to its ability to promote axonal regeneration, researchers Wang et. Al examined the potential of compound 7P to combat cervical cancer. The researchers originally hypothesized that electron-withdrawing substituents, such as compound 7P, have more potent anti-cancer qualities than electron-donating groups. Results of the study were based on the histological assessment of a mouse xenograft model inoculated with HeLa cells. It was reported that compound 7P exhibited the highest anti-cancer activity by actively inhibiting the growth of cervical tumors. Excision of the tumor-bearing tissue revealed that compound 7P improved the overall microstructure of the tissue. Furthermore, compound 7P effectively increased the amount of HeLa cells in G0/G1 and S-phases of the cell cycle while decreasing the amount of cells in the G3/M phases. Overall, this suggests the potential to activate more anti-cancer HeLa cells, however, more research should be conducted in order to determine the most effective dose (https://pubmed.ncbi.nlm.nih.gov/29068538/).

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