Synthesis and anticancer activity of di(3-thienyl)methanol and di(3-thienyl)methane

Article abstract of DOI:10.3390/molecules171011456

Di(3-thienyl)methanol (2) and di(3-thienyl)methane (3) have been synthesized and screened against the T98G (brain cancer) cell line. Treatment induced cell death (MTT and macro-colony assay), growth inhibition, cytogenetic damage (micronuclei formation), were studied as cellular response parameters. Treatment with the compounds enhanced growth inhibition and cell death in a concentration dependent manner in both T98G and HEK (normal) cell lines. At higher concentrations (>20 μ g/mL) the cytotoxic effects of the compounds were highly significant. The effect on clonogenic capacity and micronuclei formation observed after treatment of cells. Amongst the compounds, compound 2 exhibited potent activity against T98G brain cancer cells. Despite potent in vitro activity, both compounds exhibited less cytotoxicity against normal human HEK cells at all effective concentrations.

Full text of DOI:10.3390/molecules171011456

Molecules 2012, 17, 11456-11468; doi:10.3390/molecules171011456
OPEN ACCESS
molecules
ISSN 1420-3049
www.mdpi.com/journal/molecules
Article
Synthesis and Anticancer Activity of Di(3-thienyl)methanol and
Di(3-thienyl)methane
Nagendra Kumar Kaushik 1, Hong Seon Kim 2, Young June Chae 2, Young Nam Lee 2,
Gi-Chung Kwon 1, Eun Ha Choi 1 and In Tae Kim 2,*
1
Plasma Bioscience Research Center, Kwangwoon University, Seoul 139-701, Korea
2
Department of Chemistry, Kwangwoon University, Seoul 139-701, Korea
* Author to whom correspondence should be addressed; E-Mail: itkim@kw.ac.kr;
Tel.: +82-10-3795-1479; Fax: +82-2-909-1978.
Received: 2 August 2012; in revised form: 24 September 2012 / Accepted: 25 September 2012 /
Published: 27 September 2012
Abstract: Di(3-thienyl)methanol (2) and di(3-thienyl)methane (3) have been synthesized
and screened against the T98G (brain cancer) cell line. Treatment induced cell death (MTT
and macro-colony assay), growth inhibition, cytogenetic damage (micronuclei formation),
were studied as cellular response parameters. Treatment with the compounds enhanced
growth inhibition and cell death in a concentration dependent manner in both T98G and
HEK (normal) cell lines. At higher concentrations (>20 µg/mL) the cytotoxic effects of the
compounds were highly significant. The effect on clonogenic capacity and micronuclei
formation observed after treatment of cells. Amongst the compounds, compound 2
exhibited potent activity against T98G brain cancer cells. Despite potent in vitro activity,
both compounds exhibited less cytotoxicity against normal human HEK cells at all
effective concentrations.
Keywords: thienyl derivatives; T98G gliomas; HEK cells
1. Introduction
The development of new cancer therapeutic agents is one of the fundamental goals in medicinal
chemistry. One newer strategy for the research on new antimicrobial therapeutic agents has been the
use of N- and S-containing small heterocyclic compounds. In the race to synthesize new
antiproliferative drugs, thiophene derivatives have attracted a great deal of attention amongst the

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scientific community due to their therapeutic uses. The thienyl nucleus is also the core structure of a
great number of cancer growth inhibitors. Thiophene and the thienyl core have attracted the attention
of the scientific community due to their therapeutic uses as antimicrobial [1], anti HIV [2], PTP1β
inhibitors [3], tyrosine kinase inhibitor [4], antioxidant [5,6], anti-inflammatory [5,6], analgesic [5],
anti-nociceptive [6], antitubercular [7], antiarrhythemic [8], anticonvulsant [8], antiparasitic [9],
anticancer agents [10–12] and metabolic stability in cells [13]. The present work is in continuation of
our search for small medicinal active molecules and evaluation of their biological activity. In this
present study we describe anticancer activity of two dithienyl derivatives: di(3-thienyl)methanol (2)
and di(3-thienyl)methane (3) against T98G brain cancer cells. The cytotoxicity of the synthesized
compounds on normal cells were assessed using the HEK cell line, which resembles developing neuron
and neuronal stem cells and is also mentioned as good model for neuroscience studies [14]. Based on this
background, we have used HEK normal cells as a model for brain normal cells in this study.
2. Results and Discussion
2.1. Synthesis
We have synthesized di(3-thienyl)methanol (2) and di(3-thienyl)methane (3) and studied their
anticancer effects (Scheme 1 and Figure 1). The structures of compound 2 and 3 are clearly supported
by their 1H, 13C-NMR spectra and microanalysis.
Scheme 1. Synthesis of compound 2 and 3.
Reagents and Conditions: (i) n-butyllithium, ethyl formate, THF, −78 °C~RT, 1 h, 88%; (ii) NaI,
Me3SiCl, CH3CN, 0~10 °C, 0.5 h, 90%.
Figure 1. Energy minimized 3D structure of di(3-thienyl)methanol (2) and
di(3-thienyl)methane (3). Red, yellow, white color ball represents oxygen, sulfur and
hydrogen atoms respectively. Pink balls represent lone pairs on the oxygen atom.

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2.2. MTT Assay
The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cell proliferation assay
has been widely accepted as a reliable way to measure the cell proliferation rate and cell death [15,16].
The data obtained by MTT assay show that compounds 2 and 3 have inhibitory effects on the growth
of T98G and HEK cells in dosage-dependent manners. Compounds 2 and 3 can inhibit 50% T98G cell
growth (IC50) obviously in the 60–200 µg/mL range after 24, 48 and 72 h of the treatment (Figure 2).
Maximum inhibitory effect was shown by compound 2 on T98G cells after 72 h of treatment,
however compound 3 also effectively inhibits the growth of T98G cells at all the concentrations
(0.7–2,500 µg/mL) and without any time dependent effects (Figure 2). Overall compound 2 was the
most potent one, having significant a inhibitory effect on T98G cells growth. Both compounds are less
toxic to the HEK cells with 75%–97% viability at 60 µg/mL concentration at all time intervals, which
further increased by decreasing the concentration of the compounds (Figure 2). For further studies, we
have selected compound 2 on the basis of its significant toxicity against T98G brain cancer cells.
Figure 2. % Viability evaluated from MTT assay on T98G brain cancer and normal HEK
cells treated with thienyl derivative for 24, 48, and 72 h.
2.3. Growth Kinetics Assay
Figure 3 shows the growth kinetics of T98G cells treated with compound 2. Cell proliferation
kinetics have been studied at 24, 48, 72 h after compound treatment, following trypsinization and
counting total cells per plate by using a trypan blue dye and hemocytometer. Data obtained from the
growth kinetics assay shows that compound 2 has inhibitory effects on the growth of T98G cells in a
concentration dependent manner.

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Figure 3. Growth kinetics of T98G cells at 24, 48 and 72 h after treatment by compound 2
at 2.2–200 µg/mL concentrations. Untreated cells are taken as control and all values given
as mean (±SE) of three independent experiments, n = 3.
It was also noted that the cells exposed to 2.2 and 6.6 µg/mL concentrations show less growth
inhibitory effects than those treated with 20, 60 and 200 µg/mL concentration. Maximum effect was
shown by 200 µg/mL concentration of compound 2, which inhibits the growth of cells up to 93% at 48
and 72 h after treatment and its viability range was 7%–8%. In the case of 20 and 60 µg/mL exposures,
we found 45%–60% cells death at all time intervals. Cell morphology analysis revealed that shape and
size of viable cells were also affected by treatment of compound 2 (Figure 4). From Figure 4 it is
found that there was remarkable differences in shape and size of treated cells at 2.2, 20, 60 and
200 µg/mL after treatment.
Figure 4. Morphology of compound 2 treated T98G brain cancer cells at 24 h after
treatment. Cells were treated at concentration 2.2, 6.6, 20, 60 and 200 µg/mL.

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2.4. Clonogenic Assay
The clonogenic assay shows the effect of compound 2 on the colony-forming capacity and survival
of exponentially growing T98G cells. We have used the clonogenic assay for confirming the growth
inhibition results of compound 2. Clonogenic assay or colony formation assay is an in vitro assay
based on the ability of a single cell to grow into a colony. Only a fraction of seeded cells retains the
capacity to produce colonies after cytotoxic drug treatment. As observed in Figure 5, the surviving
fraction of T98G cells has been drastically decreased after its treatment by compound 2. Compound 2
treatment enhances cell death and also inhibits colony formation capability in the T98G cell population
in a concentration dependent manner. After treatments with different concentrations (2.2–200 µg/mL),
the surviving fraction of T98g cells declines, as evidenced by the reduction in the number of colonies
formed. Even at low doses, 2.2, 6.6 and 20 µg/mL exposure of compound 2 shows a significant decline
in colony survival and the surviving fractions was found to be 0.85, 0.71 and 0.58, respectively.
However, a significant drastic decline in their surviving fraction could be observed after exposure to
60 and 200 µg/mL treatment and their surviving fractions were found to be 0.32 and 0 (zero),
respectively. This shows that these treatments significantly inhibit the colony formation capabilities of
brain cancer cells at all the dosages.
Figure 5. Effect of compound 2 on colony forming capacity and survival of exponentially
growing T98G cell lines studied by macro colony assay. Data presented are mean values
from three independent observations, n = 3.
2.5. Micronucleus Assay
In recent years, the in vitro micronucleus (MN) assay has become an attractive tool for measuring
genotoxicity by physical and chemical agents, due to its capacity to detect clastogenic and aneugenic
events, simplicity of scoring, accuracy, multipotentiality and wide applicability in different cell types.
For measuring micronucleus, we have treated T98G cells with compound 2 under similar conditions
and concentrations to those which were used in earlier experiments on growth kinetics and the
clonogenic assay. After treatment by compound 2, cell cultures were grown for a 24 and 48 h in order

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to allow chromosomal damage leading to the formation of micronuclei in bi- or multinucleated
interphase cells.
Figure 6 shows the micronucleus frequency at 24 and 48 h for T98G brain cancer cell after
treatment with 2.2–60 µg/mL concentration of compound 2. The frequency of untreated cells with
micronuclei were in the range of 3.5%–3.9%; whereas the treatment with 2.2 µg/mL does not induce
any significant level of micronuclei formation in T98G cells, and the range of micronucleus is
3.8–3.9. However, micronuclei frequency increased from 3.5% (control) to 5.6%, 6.21% and 7.7% for
6.6, 20 and 60 µg/mL concentration treated cells, respectively, at 24 h of culture. However, it was
increased further at 48 h of culture as 6.6, 20 and 60 µg/mL concentrations of compound 2 further
increased micronuclei frequency from 3.9% (control) to 5.9%, 6.43% and 7.9%, respectively.
Micronuclei shown in compound 2 treated T98G cells were formed by DNA strand breaks generated
during the faulty excision repair process. The remaining unsealed DNA leads to the formation of
micronuclei in subsequent mitosis, and cells with micronuclei are found to be associated with loss of
reproductive capacity.
Figure 6. Comparison between micronucleus (MN) frequencies at 24 and 48 h in human
T98G cells treated with compound 2. Whereas ‘Control’ is micronuclei frequency of
untreated cells.Results are measured in vitro both in mononucleated cells and binucleated
cells in cultures. These cells shown with one or many micronucleus were scored for MN
frequency. The data represents mean ± SEM, n = 3.
2.6. In Silico Pharmacokinetics
For a molecule to be a probable drug, besides having a good biological activity, it must have nice
pharmacokinetic accessibility in biological systems. To access the pharmacokinetic profile of the
synthesized molecule, we used the well validated in silico tools: Osiris, Chemaxon and Catalyst. These
tools have been validated with almost 7,000 drug molecules available in market. The analysis of

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theoretical toxicity risks for the thienyl derivatives using the OSIRIS program shows that all
compounds were less toxic and can be used as a therapeutic molecules (Figure 7). As these compounds
are considered for oral delivery, they were submitted to the analysis of Lipinski ‘rule of five’,
druglikness and drug score by using the Catalyst software (Table 1).
Figure 7. In silico drug safety analysis for thienyl derivatives by Osiris software.
Our results pointed that all effective compounds fulfill this rule and their druglikness property such
as molecular weight (180–196), Log P (2.38–3.13), nHBA (0–1), nHBD (0–1) and number of rotatable
bonds (rotb) (2) were better than commercial drugs (Table 1). Finally, we evaluated thienyl derivative
2 as a potential drug by calculating druglikeness and drug-score. Druglikeness, which is related to the
similarity with trade drugs (−1.28–1.29). Drug score of all derivatives was in the range of 0.46–0.56.
Among the both thienyl compounds, 2 showed the best values of drug-score (0.56) with a lower
toxicity effect, which suggests it should be considered for further in vivo exploration.
Table 1. Pharmacokinetic parameters (Catalyst, Chemaxon and Osiris softwares).
Compounds
nHba
nHbd
nrotb
MW
196
180
cLog P Druglikeness Drug Score
2
3
1
0
1
0
2
2
2.38
3.13
−1.29
−2.28
0.56
0.47
3. Experimental
3.1. General
The MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide), bisbenzimidazole
derivative Hoechst-33342 (bis-benzimide(2-[4-ethoxyphenyl]-5-[4- methyl-1-piperazinylpiperazinyl]-
2,5-bi-1H-benzimidazole)trihydrochloride), Hank’s balanced salt solution (HBSS), Dulbecco’s
modified phosphate buffered saline (PBS), Dulbecco’s modified eagle’s medium (DMEM), fetal calf
serum (FCS), N-[2-hydroxyethyl]piperazine-N-[2-ethanesulfonic acid] (HEPES) buffer, propidium
iodide (PI), Ribonuclease-A (RNase-A), trihydro-chloride, propidium iodide and trypsin were
obtained from the Sigma Chemical Co., USA. All other chemicals used in the present study were of
analytical grade.

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3.2. Preparation of Di(3-thienyl)methanol (2)
3-Bromothiophene (1, 60 g, 0.36 mol) was added into a solution of n-butyllithium (0.36 mol) in
THF (120 mL) at −78 °C and a solution of the ethyl formate (13.63 g, 0.184 mol) in THF (60 mL) was
added dropwise while maintaining the temperature between −78 and −70 °C [17]. The mixture was
then allowed to warm slowly (over ~1 h) to RT. The resulting mixture was hydrolyzed with 10%
aqHCl (76.8 g) with cooling below 0 °C. The organic layer was separated, and the aqueous layer was
extracted with CHCl3 (300 mL × 3). The combined solutions were dried with Na2SO4 and concentrated
in vacuo. The residue was chromatographed on a short silica gel column (hexane-EA 6:1) to yield a
pale-yellow viscous oil, which solidified upon standing. Yield: 88% (31.78 g); m.p. 61–62 °C.
1H-NMR (400 MHz, CDCl3): 7.19 (dd, 2H, J = 5.0, 3.0 Hz), 7.07 (m, 2H), 6.93 (dd, 2H, J = 5.0,
1.3 Hz), 5.76 (s, 1H), 3.10 (br s, 1H); 13C-NMR (100 MHz, CDCl3): 144.71 (2C), 126.26 (2C), 125.94
(2C), 121.50(2C), 68.67. Anal Calcd for C9H8OS2:C, 55.07; H, 4.11 Found: C, 54.88; H,4.17.
3.3. Preparation of Di(3-thienyl)methane (3)
To a well stirred solution of chlorotrimethylsilane (55.34 g, 0.5094 mol) in anhydrous CH3CN (240 mL)
was added NaI (76.35 g, 0.5094 mol) in one portion. The resulting slurry was stirred for 20 min at 0 °C,
and then a solution of corresponding di(3-thienyl) methanol (2, 20 g, 0.1018 mol) in CH3CN
(150 mL) was added dropwise over 30 min to maintain the reaction temperature below 10 °C [18]. The
reaction mixture was quenched with aqueous NaOH (10.99 g in 150 mL) extracted with CH2Cl2
(300 mL × 3), washed with a saturated solution of Na2S2O3∙5H2O (150 mL), and dried over Na2SO4.
Organic solvents were removed in vacuo, and the brown residue was purified by column
chromatography (hexane) to yield the pure di(3-thienyl)methane (3) as a white solid or pale yellow oil
1
which solidified upon standing. Yield: 90% (16.51 g); m.p. 35–36 °C. H-NMR (400 MHz, CDCl3):
7.38 (dd, 2H), 7.09 (m, 2H), 4.14 (s, 2H); 13C-NMR (100 MHz, CDCl3): 140.75 (2C), 128.21 (2C), 125.42
(2C), 121.00(2C), 30.89. Anal Calcd for C9H8OS2: C, 59.96; H, 4.47 Found: C, 59.74; H, 4.19.
3.4. Human Cell Culture
T98G (brain cancer) and HEK Normal (Human Embryonic Kidney) cells were used in the present
studies were purchased from SNU (Seoul, Korea). We were culture these cell line in 75 cm2 culture
flasks (Corning, New York, NY, USA) using Dulbecco’s modified Eagle’s medium (DMEM)
supplemented with 10% fetal bovine serum, 1% nonessential amino acids, 1% glutamine, penicillin
(100 IU/mL) and streptomycin (100 mg/mL) (all from Euroclone, UK) or by distributor instructions.
All cultures were maintained at 37 °C, 95% relative humidity and 5% CO2. Prior to each cytotoxicity
test, the cells were harvested using trypsin–ethylenediaminetetraacetic acid (EDTA)–PBS solution
(with 0.25% trypsin–0.05mM according to the distributor’s instructions) and diluted at a density of
5 × 105 cells/mL in MTT assays. Stock cultures were passaged every third day after harvesting the
cells with 0.05% trypsin and seeding 8 × 103 cells/cm2 in tissue culture flasks to maintain the cells in
the exponential phase. All experiments were carried out in exponentially growing cells. The cell
suspension was seeded into 24-well plates (Corning, New York, NY, USA) at 100 µL well, and
incubated for approximately 20–24 h before tests in order to reach confluency. Before the cells were

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seeded into 24-well plates, the plates were treated with 0.01% poly-D-lysine solution (Sigma-Aldrich,
Germany).
3.5. In Vitro Cell Viability Assay
Cells were seeded in 24-well plates at a concentration of 2–4 × 103 cells/well in 200 μL of complete
media and incubated for 24 h at 37 °C in 5% CO2 atmosphere to allow for cell adhesion. All assays
were performed in two independent sets of quadruplicate tests. Control group containing without
treatment was run in each assay. Following after 24, 48 and 72 h of exposure of cells to compound,
each well will be carefully rinsed with 200 μL PBS buffer. Cytotoxicity were assessed using MTT
(3-[4,5-dimethylthiazol-2yl]-2,5-diphenyltetrazolium bromide). MTT solutions 20 μL (5 mg·mL−1dd
H2O) along with 200 μL of fresh, complete media were added to each well and plates were incubated
for 3 h [19]. Following incubation, the medium were removed and the purple formazan precipitate in
each well were sterilized in 200 μL DMSO. Absorbances were measured using microplate reader at
570 nm and results were expressed as % viability which is directly proportional to metabolic active
cell number. Percentage (%) viability was calculated as:
% Viability = OD in sample well/OD in control well × 100
3.6. Cell Growth Kinetics Assay
Cells were seeded at 7,000–10,000 cells/cm2 in 90–120 mm Petri dishes or flasks, and their
proliferation kinetics will be studied at 24, 48, 72 h after treatment by compounds, following
trypsinization and counting total cells per flask/disc by using a Neubauer hemocytometer.
3.7. Clonogenic Survival Assay
Clonogenic assay or colony formation assay is an in vitro cell survival assay based on the ability of
a single cell to grow into a colony. The colony is defined to consist of at least 50 cells. The assay
essentially tests every cell in the population for its ability to undergo “unlimited” division [20].
Clonogenic assay is the method of choice to determine cell reproductive death after treatment with
ionizing radiation, but we can also be used to determine the effectiveness of drug molecules. Only a
fraction of seeded cells retains the capacity to produce colonies before or after treatment, cells will be
seeded out in appropriate dilutions to form colonies in 1–3 weeks. After harvesting with 0.05% trypsin,
150–400 (depending on the treatment) cells will be plated 10–14 h before treatment in DMEM at 37 °C.
Cultured cells will be treated with doses 20 to 100 ug/ml of compounds. After the treatment, cells will
be incubated in dark under humidified, 5% CO2 atmosphere at 37 °C for 8–10 days to allow colony
formation. Colonies will be fixed with methanol and will be stained with 1% crystal violet. Colonies of
more than 50 cells will be counted and the surviving fraction (SF) will calculated. Clonogenic survival
curves will be constructed from three independent experiments by least-squares regression fitting
averaged survival levels.

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3.8. Micronuclei Formation
The purpose of the micronucleus assay is to detect those chemical and physical agents which
modify chromosome structure and segregation in cells [21]. For measuring micronucleus we treated
T98G cells by compound under similar conditions as we used in earlier experiments for growth
kinetics and clonogenic assay. After treatment by compound, cell cultures are grown for a 24 and 48 h
to allow chromosomal damage to lead to the formation of micronuclei in bi- or multinucleated
interphase cells. Air-dried slides containing acetic acid–methanol (1:3 V/V) fixed treated cells were
stained with Hoechst-33342 (10 µg/mL in PBS (0.1M), disodium phosphate (0.45 M) buffer
containing 0.05% Tween-20 detergent). Slides were examined under the fluorescence microscope
using an UV excitation filter. Fluorescent nuclei were visualized using a blue emission filter. Cells
containing micronuclei were counted from >1,000 cells by employing the criteria of Countrymen and
Heddle [21].
The fraction of cells containing micronuclei, called the M-fraction (%) or MN frequency was
calculated as follows:
M-fraction (%) = Nm/Nt × 100
where Nm is the number of cells with micronuclei and Nt is the total number of cells analyzed. Since,
micronuclei formation is linked to cell proliferation, the micronuclei frequencies were normalized with
respect to the cell numbers.
3.9. In Silico Pharmacokinetic Screening
To evaluate pharmacokinetic profile descriptors such as cLogP (octanol/water partition coefficient)
and LogS (water solubility) were calculated using the Osiris Property Explorer on-line system [22].
The thienyl derivatives were submitted to in silico absorption, distribution, metabolism, excretion, and
toxicity (ADMET) screening, using the Osiris program. Values of druglikeness are based on the
occurrence frequency of each fragment of the molecule in commercial drugs while the drug-score
evaluates the compound’s potential to qualify for a drug and is related to topological descriptors,
fingerprints of molecular druglikeness, structural keys and other properties such as cLog P and
molecular mass [22,23]. In silico theoretical safety analysis is also evaluated by Osiris software,
whereby a score of 1 means a drug is safe and a score < 1 means a drug molecule is theoretically toxic
in use. The pharmacokinetic profile, important for a good oral bioavailability of a compound, was also
evaluated according to the Lipinski’s ‘rule-of-five’ by using the Catalyst and Chemaxon softwares,
which analyse features that a drug should present to allow the absorption and permeation across the
membranes and states molecular weight < 500 Daltons (Da), calculated octanol/water partition
coefficient (cLogP) < 5, number of hydrogen-bond acceptors (nHba) < 10, and number of
hydrogen-bond donors(nHbd) < 5 [22,23], as well as a fifth rule added later, which infers the number
of rotatable bonds < 10.

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4. Conclusions
The obtained results for human T98G brain cancer cells were compared with Human Embryonic
Kidney (HEK) cells. The compounds were more efficacious on T98G cancer cells and are less toxic to
normal human HEK cells. These thienyl derivatives may be regarded as lead structures for a new class
of anticancer agents with both drug delivery capability because of small size and capable of
chemosensitization. Finally we can conclude that compound 2 and 3 could have the broad dosage
ranges of activity against human T98G brain cancer cells. Compound 2 shows significant toxicity on
T98G cells and the least toxicity on normal HEK cells. Compound 2 also inhibits the clonogenic
capacity of T98G brain cancer cells in a concentration dependent manner. Compound 2 presents the
overall best parameters including: (a) high activity against a brain cancer cell line, (b) low cytotoxicity
risks in HEK cells, (c) low toxic effect risks in in silico analysis, (d) good oral bioavailability
according to the Lipinski ‘rule of five’, and (e) better druglikeness and drug-score values, nearly
similar or better than some commercial drugs. Studies on the mechanism by which the compound 2
induce antiproliferative effect on T98G brain cancer cells and a wider range of other cancer cell lines
are ongoing.
Acknowledgments
The present research has been conducted by the Research Grant of Kwangwoon University in 2011
and SRC program of National Research Foundation of Korea (20100029418) in 2012. This work was
supported by the New & Renewable Energy of the Korea Institute of Energy Technology Evaluation
and Planning (KETEP) grant funded by the Korea government Ministry of Knowledge Economy
(No. 96002011003) and by Ministry of Knowledge Economy (MKE), Korea as a project, “Full color
360 degree 3D holographic video making technology”.
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Sample Availability: Samples of the compounds Di(3-thienyl)methanol and Di(3-thienyl)methane are
available from the authors.
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