Bioorganic & Medicinal Chemistry Letters 29 (2019) 1133–1137

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Bioorganic & Medicinal Chemistry Letters

journal homepage: www.elsevier.com/locate/bmcl

Design, synthesis and evaluation of novel (S)-tryptamine derivatives T

containing an allyl group and an aryl sulfonamide unit as anticancer agents
Zhenbo Guoa,1, Yiming Xua,1, Yujie Pengb, Haroon ur Rashida,c, Wei Quana, Peng Xiea,
Lichuan Wub, Jun Jianga, Lisheng Wangb, , Xu Liub,
⁎ ⁎

a
School of Chemistry and Chemical Engineering, Guangxi University, Nanning, Guangxi 530004, PR China
b
Medical College of Guangxi University, Nanning, Guangxi 530004, PR China
c
Department of Chemistry, Sarhad University of Science & Information Technology, Peshawar, KP, Pakistan

ARTICLE INFO ABSTRACT

Keywords: A series of (S)-tryptamine derivatives containing an allyl group and an aryl sulfonamide unit were designed,
Tryptamine synthesized and evaluated for their potential application as anticancer agents. The structures of the synthesized
Aryl sulfonamide compounds were characterized by 1H NMR, 13C NMR and ESI-MS spectral analyses. The target compounds were
Cell cycle arrest evaluated for their in vitro cytotoxicity against HepG2, HeLa, CNE1 and A549 human cancer cell lines. Some of
Anticancer
the synthesized compounds showed moderate to good anticancer activities against four selected cancer cell lines,
among of which 6ag was found to be the most active analogue possessing IC50 values 16.5–18.7 μM. Further
mechanism studies revealed that compound 6ag could significantly induce HepG2 cell cycle arrest at G1 phase,
promote cell apoptosis, and inhibit the colony formation as well.

Cancer has become one of the most serious threats against human
health and life all over the world, and its mortality rate surpasses heart
diseases.1 Nowadays, the progress of cancer treatment still relies on
chemotherapy in which antitumor drugs play an important role.2 Al-
though researchers made much efforts to develop new drugs to cure
cancer, still millions of cancer caused deaths are reported globally.3
Therefore, it remained a tremendous challenge for scientists to search
for effective and unexplored anticancer agents with valid potency
against tumor cells.
Tryptamine, a bicyclic heterocycle, is the most important and best-
characterized member of the indoleamine family. Tryptamine scaffold
is regarded as a privileged structure, due to its broad applications for
designing medicinal agents. The tryptamine and its analogues have
been reported to exhibit diverse pharmacological activities (Fig. 1),
such as anti-migraine,4,5 antibacterial6 and antitumour2,7. Owning to its
multiples pharmacological activities, tryptamine has been considered as
the common functional group in a set of compounds termed collectively
substituted tryptamines.
D-tryptophan (Fig. 2), a non-protein amino acid derived from
Tryptamine, possesses special physiological properties due to its optical
activity, which can serve as sweetener, feed additive and plant growth
substance etc. in various fields. Especially in pharmaceuticals, it is an
essential synthetic precursor for anticancer agents and im-
munosuppressants.8 The above suggestions urged us to perform mod-
ifications based on D-tryptophan, maintaining the chirality and trypta-
mine scaffold. On the other hand, the S-allylcysteine (Fig. 2) is
identified as a potent compound from garlic, and is reported to have
anticancer effect.9,10. An obvious characteristic is the similarity of
chiral center between D-tryptophan and S-allylcysteine. It was also
discovered that the biochemical transformation of the allyl sulfur
compounds in the cell and their adducts with thiol functional groups of
proteins, could be considered relevant events to uncover the anticancer
properties of the allyl sulfur compounds.11 Moreover, lack of allyl group
can cause the biological activity of S-allylcysteine lose.12 Thus, with the
chirality and tryptamine structure of D-tryptophan unchanged, allyl
group was primarily introduced into the D-tryptophan, forming another
analogous scaffold of S-allylcysteine, which was expected to exhibit
anticancer synergies.
Further, in considering the significant biological effect of chirality in
medicinal chemistry, the degree of selectivity was altered followed by
modification on amino position. On the other hand, sulfonamide moiety
is a core part of many clinical drugs which have broad spectrum ap-
plications in the fields of medicine, pharmacology and pharmaceutics
such as antibacterial, antiviral, anti-inflammatory, protease inhibitor,

⁎
Corresponding authors.
E-mail addresses: lswang@gxu.edu.cn (L. Wang), wendaoliuxu@163.com (X. Liu).
1
These authors have contributed equally.

https://doi.org/10.1016/j.bmcl.2019.02.023
Received 3 July 2018; Received in revised form 13 February 2019; Accepted 20 February 2019
Available online 20 February 2019
0960-894X/ © 2019 Elsevier Ltd. All rights reserved.
Z. Guo, et al. Bioorganic & Medicinal Chemistry Letters 29 (2019) 1133–1137

Fig. 1. Pharmaceutically important tryptamine analogues.

Fig. 2. Chemical structure of S-allylcysteine, Terrequinone A and Indisulam.

anti-diabetic, anti-cancer, anti-epileptic and anti-tumor etc.13 For ex-

ample, indisulam (Fig. 2) is an aryl sulfonamide drug with anticancer
activity, which caused cell cycle arrest in G1 phase, followed by cell
death.14 SAR analysis of indisulam indicated that sulfonamide group is
essential for antitumor properties of indisulam. More importantly, the
aryl group and substituent are particularly important for the mitotic
arrest phenotype.15 Souvik Banerjee’s et al.16 discovered an aryl sul-
fonamide drug which significantly reduced B16 melanoma metastasis in
vivo. More remarkably, Yoshinori et al. synthesized a series of N-Sul-
fonyl D-tryptophan derivatives and revealed that their inhibitory ac-
tivities were greatly affected by the introduction of the sulfonamide
moiety into amino group as novel candidates for the treatment of
Scheme 1. Synthetic route for (S)-tryptamine derivatives. Reaction conditions:
cancer.17
(a) dry diethyl ether, oxalyl chloride, 0 °C → rt, 6 h, methanol, 0 °C, 30 min; (b)
Herein, aryl sulfonamide was then introduced into amino group to
LiAlH4, dry THF, N2, 0 °C, 1 h and then 70 °C, 4 h; (c) DMSO, IBX, N2, rt, 90 min;
synthesize a series of (S)-tryptamine derivatives (Fig. 3). Subsequently, (d) dry THF, Indium powder; (SR)-N-tert-butanesulfinamide, Ti(OEt)4, N2,
the derivatives were evaluated for their anticancer activities via in vitro 23 °C, 3 h; allylic bromide; 60 °C, 20 h; (e) dry 1,4-dioxane/dry methanol = 1:1,
cytotoxicity assay against cancer cell lines (HepG2, HeLa, CNE1 and anhydrous HCl in dioxane, rt, 1 h; (f) TEA, DCM, rt, overnight; (g) ethanol,
A549). Furthermore, the mechanism of action of compound 6ag against FeCl3·6H2O, aqueous hydrazine, rt, 4 h.
liver cancer cell (HepG2) was also investigated.
The synthetic route of the new analogs 6a-6al is illustrated in
method.22 However, the yield was reported to be very low. Therefore,
Scheme 1. The preparation of intermediate 1 was performed by fol-
further optimization of the reaction conditions was carried out via
lowing the procedure reported previously.18,19 Indole was allowed to
Maoqun Tian’s method.23 A mixture of compound 4, (SR)-N-tert-buta-
react with oxalyl chloride in dry diethyl ether followed by the addition
nesulfinamide, indium powder, and Ti(OEt)4 was allowed to react in
of methanol to yield the methyl 2-(1H-indol-3-yl)-2-oxoacetate (1).
dry tetrahydrofuran at 23 °C for 3 h, and was then treated with allylic
Then, the intermediate 1 was allowed to react with LiAlH4 in dry tet-
bromide at 60 °C for 20 h. Consequently, a mixture of two diastereoi-
rahydrofuran to afford 2-(1H-indol-3-yl)ethan-1-ol (2).20 Subsequently,
somers of 4 (dr = 2:1) was obtained, which was separated by silica gel
2-(1H-indol-3-yl)ethan-1-ol (2) was oxidized by 2-Iodylbenzoic acid in
flash column chromatography and a single isomer 4 was obtained in
dimethyl sulfoxide to afford 2-(1H-indol-3-yl)acetaldehyde (3), a ra-
moderate yield. This key chiral compound 4 was then treated with
pidly decomposing aldehyde and was therefore used for the next step
anhydrous HCl in a mixture of solvents consisted of dry 1, 4-dioxane
immediately after workup.21
and dry methanol (1:1). Consequently, tert-butanesulfinyl group of
Attempts were made to synthesize compound 4 by the José’s
chiral 4 was eliminated and compound 5 was afforded in 90% yield.24
Single crystals of compound 5 were obtained by recrystallization in
chloroform and the absolute structure was further confirmed to be S by
X-ray diffraction determination (Fig. 4). Crystallographic data of 5 have
been deposited at the Cambridge Crystallographic Data Centre (CCDC)
with deposition numbers of 1812759.
In order to testify the rationality of design, two modification stra-
tegies were adopted. Compound 5 was firstly allowed to react with
arylsulfonyl chloride in CH2Cl2 in the presence of trimethylamine,
yielding the target compounds 6a-6am. On the other hand, compound 7
Fig. 3. Target compounds designing. was prepared by reduction of 5 via aqueous hydrazine in the presence

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Z. Guo, et al. Bioorganic & Medicinal Chemistry Letters 29 (2019) 1133–1137

Table 1
Cytotoxic activities assays of compounds 6a-6al against HepG2, HeLa, CNE1
and A549 cell lines.
Compound IC50 (μM)a Clog Pc

HepG2b HeLab CNE1b A549b

6a > 100 > 100 NTd NT 4.336

6b 38.2 ± 4.3 33.8 ± 2.6 34.2 ± 3.1 41.6 ± 4.1 5.155
6c 33.2 ± 4.3 46.9 ± 5.3 34.2 ± 3.9 50.7 ± 4.9 5.335
Fig. 4. Perspective drawing of the X-ray crystal structure of 5. 6d 36.3 ± 5.1 32.0 ± 1.9 27.0 ± 3.2 38.5 ± 4.2 5.552
6e > 100 > 100 NT NT 4.606
6f 71.7 ± 7.5 61.7 ± 6.5 NT NT 4.855
of a catalytic amount of FeCl3·6H2O.25 Finally, target 8a-8b were pre- 6g 55.4 ± 2.3 41.1 ± 4.8 42.7 ± 4.6 55.7 ± 5.2 5.425
pared according to the synthesized process of compounds 6a-6am. 6h 54.3 ± 5.2 53.5 ± 3.8 38.5 ± 4.0 48.8 ± 4.4 5.575
Based on the X-ray crystallographic structure analysis of 5, absolute 6i 78.4 ± 9.2 74.4 ± 6.2 NT NT 5.155
configuration of 6a-6am and 8a-8b were determined. All the synthe- 6j 71.3 ± 9.8 67.9 ± 7.8 NT NT 4.921
6k 89.7 ± 9.1 53.2 ± 4.2 NT NT 4.921
sized compounds were purified by silica gel flash column chromato-
6l 24.4 ± 2.7 42.8 ± 4.4 28.8 ± 2.6 34.3 ± 4.1 5.922
graphy using ethyl acetate and petroleum ether as gradient eluents and 6m 58.9 ± 8.4 40.5 ± 2.1 48.0 ± 2.4 52.1 ± 6.3 5.056
their structures were characterized by 1H NMR, 13C NMR and ESI-MS 6n 39.6 ± 3.9 61.0 ± 6.8 41.2 ± 4.3 58.6 ± 5.9 5.056
spectral analyses. 6o 58.1 ± 6.8 54.5 ± 3.3 NT NT 5.305
After synthesis and characterization of the target compounds, their 6p 58.7 ± 6.7 58.5 ± 6.2 NT NT 5.305
6q 35.3 ± 4.3 58.9 ± 5.6 43.4 ± 2.4 65.0 ± 9.1 5.485
cytotoxic activities were determined against four different cancer cell 6r 52.2 ± 4.1 46.7 ± 4.2 38.6 ± 4.1 54.1 ± 4.5 5.555
lines viz. HepG2, HeLa, CNE1 and A549. The viability of the cell was 6s 51.8 ± 5.1 41.7 ± 5.3 38.1 ± 2.9 49.9 ± 4.9 5.303
assessed by the MTT assay in vitro.26 Cisplatin was used as a positive 6t 33.1 ± 2.0 44.8 ± 3.8 36.1 ± 3.2 53.0 ± 6.0 5.822
control which showed IC50 values of 4.9 ± 0.2 μM for HepG2, 6u 42.1 ± 3.3 39.3 ± 4.5 34.4 ± 2.1 43.9 ± 3.6 5.772
6v 40.4 ± 1.3 35.7 ± 2.6 39.3 ± 4.6 74.2 ± 6.2 5.170
10.0 ± 1.1 μM for Hela, 2.5 ± 0.3 μM for CNE1 and 16.3 ± 2.1 μM
6w 46.9 ± 3.9 45.1 ± 3.5 40.7 ± 4.4 52.1 ± 5.1 5.303
for A549 cancer cell lines. The anticancer potency of these compounds 6x 25.3 ± 2.1 31.9 ± 2.1 22.9 ± 2.5 29.3 ± 1.9 6.272
as half maximal inhibitory concentration (IC50) values represented the 6y 21.9 ± 2.0 30.2 ± 3.1 24.1 ± 2.1 35.6 ± 4.4 6.371
compound concentration which causes a 50% reduction of cell growth. 6z > 100 > 100 NT NT 4.390
The IC50 values of target compound are summarized in Table 1. 6aa 39.1 ± 3.5 43.6 ± 4.7 39.8 ± 4.3 70.2 ± 8.9 4.835
6ab 44.6 ± 8.4 45.6 ± 3.0 42.0 ± 2.0 48.3 ± 5.5 4.889
The cytotoxic activity results indicated that most of the synthesized
6ac 37.2 ± 4.2 35.3 ± 5.1 31.5 ± 3.2 40.4 ± 2.8 5.388
compounds exhibited anticancer activity with IC50 below 100 μM, while 6ad 24.7 ± 2.3 26.1 ± 3.5 26.3 ± 3.2 29.9 ± 3.1 5.787
some showed potent activity with IC50 below 50 μM against four se- 6ae 58.4 ± 5.6 67.1 ± 7.3 NT NT 5.448
lected cancer cell lines, respectively. Among the synthesized com- 6af 46.4 ± 4.2 43.5 ± 2.4 43.6 ± 3.0 53.0 ± 5.2 5.318
6ag 16.5 ± 1.2 16.5 ± 1.1 18.3 ± 1.6 18.7 ± 1.5 8.172
pounds, compound 6ag was found to be the most potent derivative
6ah 43.0 ± 3.6 34.5 ± 2.1 34.5 ± 3.0 33.6 ± 2.9 5.779
against HepG2, HeLa, CNE1 and A549 with IC50 values of 6ai 44.89 ± 4.8 52.7 ± 5.9 45.2 ± 5.1 55.5 ± 6.1 5.065
16.5 ± 1.2 μM, 16.5 ± 1.1 μM, 18.3 ± 1.6 μM, 18.7 ± 1.5 μM re- 6aj 52 ± 5.3 34.5 ± 3.6 36.0 ± 3.5 52.4 ± 5.4 5.390
spectively, which showed equivalent efficacy with Cisplatin in regard to 6ak 36.0 ± 4.1 57.3 ± 6.2 39.9 ± 2.5 57.8 ± 5.7 5.278
HeLa and A549 cells. 6al 39.5 ± 4.2 68.2 ± 5.6 66.9 ± 7.2 65.9 ± 4.8 4.798
6am 58.4 ± 4.8 69.5 ± 5.3 40.8 ± 3.7 77.1 ± 6.2 3.891
As expected, most compounds of 6a-6am series showed better an-
8a 68.7 ± 5.5 78.9 ± 4.8 47.1 ± 3.5 91.5 ± 7.8 4.375
ticancer activity than 5, which indicated aryl sulfonamide group played 8b 30.8 ± 2.4 16.4 ± 0.9 17.8 ± 1.0 39.8 ± 3.3 8.656
an important role in enhancing activity. 5 > 100 > 100 > 100 > 100 2.306
Thus, the SAR studies were first focused on the substituents on the 7 > 100 > 100 > 100 > 100 2.79
Cisplatin 4.9 ± 0.2 10.0 ± 1.1 2.5 ± 0.3 16.3 ± 2.1
phenyl group of R. Through comparing the anticancer results of 6a-6al
with 6am, it can be observed that presence of electron-withdrawing or a
IC50 values are indicated as the mean ± SD of three independent experi-
electron-donating substituent groups on aryl could not promote activity ments. The cells were continuously treated with compounds for 48 h.
to produce a single effect. In other words, electronic effect may not be b
Cells lines include human liver cancer cell line (HepG2), cervix cancer cell
the determinant for activity. Moreover, among 6a-6y with electro- line (HeLa), nasopharyngeal cancer cell line (CNE2), lung cancer cell line
ndrawing group, the compounds possessed -CF3 group generally ex- (A549).
hibited potent anticancer activity, such as 6d, 6l, 6t, 6u 6x and 6y. On c
ClogP values produced by Chemdraw software.
d
the other hand, compounds 6ad and 6ag showed the most potent ac- NT means not tested.
tivity among 6aa-6al. An obvious characteristic is that trifluoromethyl,
2, 3,5,6-tetra-methyl (6ad) and 2,4,6-tri-isopropyl (6ag) groups could 8a and 8b were synthesized and tested for cytotoxic activity. With 6am,
significantly improve lipotropy. The aforementioned results lead us to 6ag as a reference, 8a and 8b showed lower activity than 6am and 6ag,
the following assumptions that lipophilic effect may be due to the respectively, which revealed the allyl group was beneficial for antic-
substituent group which in turn is responsible for enhancement of cy- ancer activity.
totoxic activity. It can be observed that, the Clop values of compounds In general, the aryl sulfonamide and allyl moieties were necessary in
6d, 6l, 6t, 6u, 6x, 6y, 6ad and 6ag are larger than other compounds, the tryptamine derivatives for anticancer activity and the lipotropy
indicating that compounds 6d, 6l, 6t, 6u, 6x, 6y, 6ad and 6ag are caused by the substituents on aryl sulfonamide have a vital role in
comparatively more lipophilic. Hydrophobicity, known as a funda- anticancer improvement. Since compound 6ag afforded a potent an-
mental pharmacological parameter, could influence the absorption of ticancer activity, it was chosen as a representative to further carry out
medicine, biological activities, interactions with receptors and the its mechanism of action of cytotoxic activities study.
toxicity resulting from molecular metabolism etc. This may be the We selected colony assay to investigate whether compound 6ag
reason for better antiproliferative activities of compounds 6d, 6l, 6t, 6u, could inhibit the proliferation of HepG2 cells (Fig. 5A and B). Compared
6x, 6y 6ad and 6ag. to the control, HepG2 cells treated with the compound 6ag exhibited
Finally, SAR analysis was focused on allyl group. In order to un- fewer colonies with 95% inhibitions at 7.5 μM, indicating that com-
derstand whether allyl group could take effect on activity, compounds pound 6ag could inhibit the proliferation of cancer cells in a dose

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Fig. 5. (A) Images of HepG2 cells colonies after treatment with compound 6ag at 0, 2.5, 5 and 7.5 μM for 2 weeks. (B) The rate of inhibition induced by compound
6ag was expressed as the mean ± SD. The clonogenicity assay was quantified using Image J software (*P < 0.05, **P < 0.01).

Fig. 6. Compound 6ag induced apoptosis in HepG2 cells. (A) HepG2 was treated with compound 6ag at 0, 10, 20 and 30 μM for 48 h. (B) HepG2 apoptosis rates were
quantified by flow cytometry. Three individual experiments were performed for each group. The data were expressed as the Mean ± SD. **p < 0.01, ***p < 0.001
compared to the control. Concentration of compound 6ag.

dependent manner. V-FITC/PI double staining and were then quantified by flow cytometry
To explore the detail cytotoxic effect of 6ag on HepG2 cells, we analysis (Fig. 6A and B). The results showed that, the percentage of
determined the effect of 6ag on cell apoptosis.27 HepG2 cells treated HepG2 apopotic cells (Lower right quadrant, AV+/PI and Upper right
with 0 μM, 10 μM, 20 μM and 30 μM of 6ag, were subjected to Annexin quadrant, AV+/PI + ) significantly increased from 4.91% to 9.61%,

Fig. 7. Compound 6ag could induce G1 cell cycle arrest in HepG2 cancer cells. (A) 6ag induces G1 cell cycle arrest in HepG2 cells in a dose-dependent manner. (B)
Distributions of G1, S and G2 in HepG2 cells under 6ag treatment.

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26.14%, 73.71% at 0 μM, 10 μM, 20 μM, 30 μM of 6ag concentrations (guijiaoren (2014) 49 hao).
treatment, respectively after 48 h incubation.
To establish whether 6ag inhibited cell growth by interrupting the Appendix A. Supplementary data
cell cycle progress, cellular DNA was analyzed and stained with pro-
pidium iodide (PI). Flow cytometry was then applied to analyze the Supplementary data to this article can be found online at https://
cells. The profiles are shown in Fig. 7(A and B). Obviously, compared to doi.org/10.1016/j.bmcl.2019.02.023.
the control group, an increase in the G1 population of HepG2 cells was
observed after treatment with 6ag at a dose of 0, 15, 25 and 35 μM for References
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