Biological evaluation of chalcones and analogues as hypolipidemic agents

Article abstract of DOI:10.1002/ardp.200600034

In order to evaluate the anti-hyperlipidemic effect of synthetic chalcones and some analogues, nineteen compounds with different substituents in both rings were synthesized and hypolipidemic activities were measured in vivo using Triton WRl339 acute and hypercaloric chronic assays. 4′,4- dichlorochalcone, 3′,4′,4-trichlorochalcone, and 4′-chlorochalcone gave an excellent decrease in serum total cholesterol and triglycerides in the acute assay. These compounds also showed significant anti-lipidemic activity in the chronic assay.

Full text of DOI:10.1002/ardp.200600034

Arch. Pharm. Chem. Life Sci. 2006, 339, 541–546
L. Santos et al.
541
Full Paper
Biological Evaluation of Chalcones and Analogues as
Hypolipidemic Agents
Lorena Santos1, Rozangela Curi Pedrosa1, Rogꢀrio Correa2, Valdir Cechinel Filho2,
Ricardo Josꢀ Nunes3, and Rosendo Augusto Yunes3
1 Departament of Biochemistry, Universidade Federal de Santa Catarina -UFSC, Florianopolis, Brazil
2 Nucleo de Investigaꢀꢁes Quꢂmico FarmacÞuticos (NIQFAR), Universidade do Vale do Itajaꢂ (UNIVALI),
Itajaꢂ, Brazil
3 Post Graduation in Chemistry, Universidade Federal de Santa Catarina (UFSC), Florianꢃpolis, Brazil
In order to evaluate the anti-hyperlipidemic effect of synthetic chalcones and some analogues,
nineteen compounds with different substituents in both rings were synthesized and hypolipide-
mic activities were measured in vivo using Triton WR1339 acute and hypercaloric chronic assays.
49,4-dichlorochalcone, 39,49,4-trichlorochalcone, and 49-chlorochalcone gave an excellent decrease
in serum total cholesterol and triglycerides in the acute assay. These compounds also showed
significant anti-lipidemic activity in the chronic assay.
Keywords: Chalcones analogues / Cholesterol / Hypolipidemic activity / Triglycerides /
Received: February 21, 2006; accepted: April 24, 2006
DOI 10.1002/ardp.200600034
estrogenic, antifungal, antinociceptive, antibacterial,
antiviral, and anti-inflammatory [3, 4]. Their antifungal
and antileishmanial activities suggest that the mode of
action of some chalcones is by inhibiting the activity of
an enzyme that participates in the biosynthesis of ergos-
terol [5, 6]. In this study, we tested the hypolipidemic
effects of chalcones in rats.
Introduction
Today, coronary artery disease and the atherosclerotic
process with which it is closely associated constitute the
major cause of death in Western society, and hypercho-
lesterolemia is a major and modifiable risk factor for cor-
onary heart disease [1]. Low serum high-density lipopro-
tein cholesterol (HDL-C) levels together with an increase
in the level of total cholesterol, low-density lipoprotein
cholesterol (LDL-C) and triglycerides are strong predictors
of coronary heart disease [2]. The cause of hyperlipidemia
is thought to be related to increased lipid synthesis,
decreased lipid clearance from the blood, or a combina-
tion of these two processes.
Chalcones are natural compounds belonging to the fla-
vonoid family. Chemically, they consist of open-chain fla-
vonoids in which the two aromatic rings are joined by a
three-carbon a-, b-unsaturated carbonyl system. They
carry out biological activities, the most important being
Results and discussion
As shown in Scheme 1 and Table 1, nineteen chalcones
were synthesized by a base-catalyzed condensation of
appropriate acetophenones and aldehydes. 2,3-dibromo-
1,3-diphenylpropanones were obtained by reacting the
appropriate chalcones with bromide. All synthesized
compounds were screened for hypolipidemic activity in
an acute experimental model and then some of these
were screened in a chronic experimental model.
The concentrations of total cholesterol, VLDL-choles-
terol and triacylglycerides in the acute assay showed that
all compounds tested were able to decrease total serum
cholesterol as shown in Table 2.
Some chalcones were selected for the chronic assay
according to the results obtained in this screening test
Correspondence: Rozangela Curi Pedrosa, Centro de CiÞncias Biolꢃgi-
cas, Laboratꢃrio de Bioquꢂmica Experimental-Departamento de Bioquꢂmi-
ca, Universidade Federal de Santa Catarina, CEP: 88040-900 Florianꢃ-
polis, SC, Brazil.
E-mail: roza@ccs.ufsc.br
Fax: +55 48 331-9672
i 2006 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim

542
L. Santos et al.
Arch. Pharm. Chem. Life Sci. 2006, 339, 541–546
Scheme 1. Synthesis of chalcones (A) and
related compounds (B), with substitutions
(X), (Y), and (n), according to the method
previously described by Guider et al. [12].
Novel syntheses were indicated as ns.
Table 1. Synthesized chalcones and related compounds.
hepatic cholesterol and triglycerides in the model of
chronic hyperlipidemia (Tables 3 and 4). The AAI% (anti-
atherogenic index), a measure of the antiatherogenic
potential of a given drug, was significantly higher in the
groups treated with 2 and 5 chalcones. These results sup-
port the hypothesis that the chalcones expresses hypoli-
pidemic activity in vivo in acute and chronic assays.
The most active compounds in the acute assay were
49,4-dichlorochalcone 2, 39,49,4-trichlorochalcone 5, and
49-chlorochalcone 7; they decreased total serum choles-
terol by 78, 72, and 79%, and triglycerides by 94, 65, and
89%, repectively. Furthermore, these compounds exhib-
ited antilipidemic activity in the chronic assay, decreas-
ing the total serum cholesterol by 70, 77, and 69%, and
triglycerides by 83, 75, and 84%, respectively.
The 49,4-dichlorochalcone also gave a greater reduction
in LDL-C and VLDL-C and a greater increase in the HDL-C
concentration with respect to the unsubstituted com-
pound. It is important to note that the AAI% of this com-
pound was higher than that of lovastatin, a specific inhi-
bitor of the rate-limiting enzyme of cholesterol synthesis,
3-hydroxy-3-methylglutaryl coenzyme-A (HMG-CoA)
reductase. However, it must be noted that 49,4-dichloro-
chalcone was used in a molar ratio of 5:1 with respect to
lovastatin.
Compounds (A)
X
Y
Reference
1
2
3
4
5
6
7
10
11
12
13
14
49-H
4-H
4-Cl
4-Cl
4-H
4-H
4-H
4-Cl
4-CH3
4-NO2
4-OCH3
2-OCH3
3-OCH3
18
3
3
3
3
49-Cl
49-Br
49-Br
49-Cl
3‘,49-Cl
3‘,49-Cl
49-H
3
3
19
20
20
ns
19
4-H
49-H
49-H
49-H
Compounds (B)
8
9
15
49-OCH3
29-OH
49-H
4-H
4-H
4-H
ns
ns
ns
Compounds (C)
16
17
18
19
49-Cl
49-H
49-H
49-H
4-Cl
ns
ns
ns
ns
4-CH3
4-NO2
4-OCH3
(Triton WR1339). Hence, the compounds (1, 2, 3, 4, 5, 7,
11), which simultaneously decreased cholesterol (72%)
and triglyceride levels (58%), along with compounds 13
and 17, which gave a large reduction in cholesterol levels
(80 and 51%) in spite of a low reduction in triglyceride
(34 and 31%) were selected for the second experimental
model. Thus, the other compounds were not tested in the
chronic assay.
According to Garattini et al. [7], a decrease in hyperlipe-
mia 8 h after intraperitoneal (i.p.) administration of a
drug, given at the same time as Triton WR1339 there is
evidence of activity resulting from the inhibition of cho-
lesterol and fatty acids synthesis. Furthermore, previous
studies have shown that in vivo inhibition of lipoprotein
lipase with Triton WR1339 blocks VLDL catabolism, inhi-
The chalcones tested lowered the serum levels of total
cholesterol, triglycerides, LDL-C, and VLDL-C, as well as
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Arch. Pharm. Chem. Life Sci. 2006, 339, 541–546
Syntheses and Evaluation of Chalcones and Analogues
543
Table 2. Effect of the tested chalcones (12.5 mmol/kg, b.w.), VLDL-cholesterol, and lovastatin (2.5 mmol/kg, b.w.) on serum total
cholesterol (TC) and triglyceride (TG) levels and control group results in acute Triton WR1339 assays.
Compound
TC
(mg/dL)
TC
TG
(mg/dL)
TG
VLDL-C
(mg/dL)
VLDL-C
Reduction
(%)a)
Reduction
Reduction
(%)a)
(%)a)
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
57.6 l 12.8***
45.4 l 4.6***
53.9 l 7.7***
45.6 l 5.8***
66.3 l 7.4***
100.2 l 13.6***
43.4 l 6.9***
76.4 l 8.4***
53.2 l 7.2***
47.0 l 7.2***
44.0 l 6.7***
68.8 l 6.4***
40.8 l 7.1***
53.7 l 20.0***
74.7 l 16.6***
64.9 l 13.0***
100.7 l 10.4***
79.8 l 9.8***
55.6 l 6.9***
72.4 l 3.4***
98.6 l 7.4
72
78
74
78
72
51
79
63
74
77
79
66
80
74
64
58
51
61
73
65
–
228.9 l 9.6***
30.2 l 4.4***
39.1 l 5.4***
37.0 l 11.8***
190.7 l 9.2***
447.5 l 5.8***
57.1 l 4.4***
438.6 l 19.4***
331.1 l 13.1***
442.5 l 16.1***
37.8 l 10.1***
396.4 l 19.1***
359.1 l 7.7***
307.7 l 18.5***
277.6 l 11.9***
105.9 l 10.5***
371.5 l 8.2***
104.6 l 10.2***
760.8 l 14.3
632.5 l 25.3**
96.46 l 3.4
58
94
93
93
65
17
89
19
39
18
93
27
34
43
49
65
31
65
–
45.8 l 9.6
6.0 l 4.4***
7.8 l 5.4***
7.4 l 11.8***
38.1 l 10.2
89.5 l 5.8
11.4 l 4.4***
87.7 l 19.4
66.2 l 13.1
88.5 l 16.1
7.6 l 10.1***
73.9 l 19.1
71.8 l 7.7
61.5 l 18.5
55.5 l 11.9
16.2 l 10.5**
74.3 l 8.2
16.3 l 10.4**
152.2 l 14.3
126.5 l 25.3
19.3 l 3.4
58
94
93
93
65
17
89
19
39
18
93
32
34
43
49
85
31
85
–
17
18
19
Lovastatin
Normal control
–
–
–
–
Triton WR-1339 control 205.4 l 10.3
–
541.6 l 23.9
–
108.3 l 23.9
–
Table 3. Lowering effect of the tested chalcones (12.5 mmol/kg, b.w.) and lovastatin (2.5 mmol/kg, b.w.) on serum total cholesterol
(TC), serum triglycerides (TG), hepatic cholesterol (HC), and hepatic triglycerides (HTG) levels and control group results in chronic
hyperlipemia diet assay.
Compound
TC
(mg/dL)
TC
TG
TG
Reduction (mg/mg
(%)a)
protein)
HC
HC
Reduction (mg/mg
(%)a)
protein)
HTG
HTG
Reduction (mg/dL)
Reduction
(%)a)
(%)a)
1
2
3
4
5
7
11
13
49.4 l 9.3*** 71
49.9 l 9.8*** 70
65.6 l 7.1*** 31
70.2 l 2.9*** 58
39.1 l 2.3*** 77
52.4 l 3.9*** 69
47.7 l 8.0*** 71
52.3 l 7.8*** 69
95.0 l 6.7*** 43
69.6 l 4.9*** 58
30.9 l 7.3*** 93
38.2 l 0.5*** 60
18.0 l 0.2*** 85
407.4 l 3.3*** 51
205.7 l 4.6*** 69
57.0 l 9.6*** 83
112.5 l 9.7*** 61
104.7 l 6.8*** 67
89.1 l 9.6*** 75
45.3 l 3.9*** 84
71.8 l 5.8*** 80
85.9 l 7.4*** 77
81.4 l 6.9*** 64
54.2 l 9.7*** 71
–
–
–
–
–
–
–
–
25.9 l 1.8*** 79
30.4 l 0.5*** 75
205.6 l 2.6*** 69
395.9 l 5.1*** 46
–
–
–
–
–
–
–
–
–
–
–
–
17
Lovastatin
54.1 l 0.6*** 55
429.5 l 5.7*** 54
Normal
Hyperlipemic control
97.0 l 6.8
167.8 l 3.6
–
–
67.1 l 5.9
188.7 l 4.3
–
–
52.7 l 0.9
121.6 l 1.8
–
–
244.9 l 5.1
672.6 l 4.8
–
–
a)
Percent reduction compared to hyperlipemic control group. Each group was composed of six rats and the determinations were
performed in duplicate. All values were expressed in terms of mean l SEM. *** indicates statistical significance in relation to
hyperlipemic control group, P a 0.001.
biting the degradation of VLDL particles and causing cone is an inhibitor of some enzyme involved in ergos-
accumulation of blood VLDL particles rich in triglycer- terol biosynthesis [6], suggest that the mode of action of
ides formed in the liver [8]. These and previous results, these chalcones in their hypocholesterolemic effect
which have shown that 29,69-dihydroxy-49-methoxychal- could be associated with the inhibition of an enzyme
i 2006 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
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544
L. Santos et al.
Arch. Pharm. Chem. Life Sci. 2006, 339, 541–546
Table 4. Effect of the tested chalcones (12.5 mmol/kg, b.w.) and lovastatin (2.5 mmol/kg, b.w.) on total cholesterol (TC), high density
lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), and antiatherogenic index (AAI) in chronic assay (hyper-
lipemic diet).
Compound
HDL-Cholesterol
(mg/dL)
LDL-Cholesterol
(mg/dL)
VLDL-C
(mg/dL)
AAI
(%)
1
2
3
4
5
7
11
13
20.4 l 8.9**
42.8 l 3.5
35.5 l 6.5
27.9 l 4.2*
26.9 l 4.4*
33.9 l 3.5
16.5 l 1.9***
15.3 l 2.2***
23.2 l 7.4**
57.9 l 3.9
31.0 l 3.6
81.6 l 2.1
32.8 l 4.2***
18.5 l 5.6***
52.6 l 1.5***
63.2 l 0.1***
30.0 l 3.9***
27.6 l 0.3***
45.7 l 4.9***
49.0 l 4.2***
88.1 l 2.3***
22.5 l 1.5***
89.4 l 1.3
17.8 l 9.6
11.4 l 10.6
22.5 l 10.0
20.9 l 6.8
17.8 l 9.6
9.06 l 3.9
14.4 l 5.8
17.2 l 7.4
16.3 l 6.9
10.8 l 12.7
13.4 l 5.9
37.7 l 4.3
70.6 l 0.5
602.8 l 7.7
117.9 l 0.6
65.9 l 1.4
222.3 l 2.1
183.2 l 0.5
52.7 l 6.1
41.3 l 5.6
32.3 l 0.6
495.6 l 1.0
–
17
Lovastatin
Control
Hyperlipemic control
124.1 l 1.3
–
Each group was composed of six rats and the determinations were performed in duplicate. All values are expressed in terms of
mean l SEM.
***, **, * indicate statistical significance in relation to hyperlipemic control group, P a 0.001, P a 0.01, P a 0.05, respectively.
that participates in cholesterol biosynthesis. Further
studies are necessary to define clearly the precise
Experimental
Materials
mechanism of action.
All chemicals were of the highest commercially available purity.
Diagnostic kits for total cholesterol, HDL-cholesterol, and trigly-
ceride determinations were purchased from Sigma Chemical
Co. (St. Louis, MO, USA). All other reagents were purchased from
Aldrich-Chemie (Steinheim, Germany).
Reduced triglyceride and VLDL-C levels could result
also from decreased secretion and/or increased rates of
catabolism. It is important to note that the hypotrigly-
ceridemic activity of some tested chalcones was very
strong and a study group of the European Atherosclerosis
Society has recommended that more attention must be
General procedure for the preparation of chalcones
paid to hypertriglyceridemia as a risk factor for coronary 1–20 and their bromide derivatives
Compounds 1–20 were obtained by reaction of acetophenone
heart disease [9].
and benzaldehyde (1:1) in the presence of sodium hydroxide
and ethanol and further addition (to cool) of diluted acetic acid,
according the method previously described by Guider et al. [12].
The respective products were recrystallized from ethanol. All
compounds were synthesized in good yields (55–98%) and char-
acterized by H-NMR, IR, and microanalyses. TLC using several
solvent systems of different polarity was used to determine the
purity of these compounds.
Conclusion
1
The development of an anti-hyperlipidemic agent to
lower blood total cholesterol and triglycerides simulta-
neously is important in the management of hyperlipi-
demic patients [10, 11]. This study suggests that chal-
cones, especially 49,4-dichlorochalcone, may be used as a
reference in the search for new active molecules for the
treatment of hyperlipidemia, since they cause a decrease
in total cholesterol, triglyceride, and LDL-C levels.
Chemical characterization
Melting points (m.p.) were obtained on a MELTEMPII apparatus
(Laboratory Devices, USA) and were uncorrected. Infrared (IR)
spectra were recorded on a Perkin-Elmer 597 infrared spectro-
photometer (Perkin Elmer, Wellesley, MA, USA). Proton nuclear
magnetic resonance (1H-NMR) spectra were obtained with a Bru-
ker Nuclear AC-200F 80 MHz and a Bucker 400 MHz spectro-
meter (Bruker BioSpin GmbH, Karlsruhe, Germany). Chemical
shifts are reported in parts per million (d) relative to tetra-
methylsilane (TMS) and signals are given as follows: s: singlet; d:
doublet; t: triplet; m: multiplet. Elemental analyses were per-
formed with a Perkin-Elmer 2400 CHN analyzer. Percentages of
C and H were in agreement with the product formula (within l
0.4% of theoretical values). The novel compounds synthesized to
our best knowledge are the following:
The authors wish to thank the Nucleo de Investigaꢀꢁes Quꢂ-
mico FarmacÞuticos (NIQFAR) of Universidade do Vale de Itajaꢂ
for chemical syntheses of the chalcones examined and the Cen-
tral Analysis Laboratory of the Chemistry Department of Uni-
versidade Federal de Santa Catarina for the physico-chemical
analyses. The authors are grateful to CNPq and FAPESC for
financial support.
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Arch. Pharm. Chem. Life Sci. 2006, 339, 541–546
Syntheses and Evaluation of Chalcones and Analogues
545
(2E,4E)-1-(49-Methoxybenzoyl)-4-phenylbutadiene 8
MW = 264 g; m.p.: 84–868C; yield: 80%; FT-IR (KBr disk, cm– 1):
1653 (m C=O), 1602 (m C=C); H1-NMR (DMSO-d6, ppm): 3.86 (s, 3H,
OCH3), 7.09 (d, 2H, H39, H59, J = 8), 7.22–7.62 (m, 5H, H2–H6),
7.37 (d, 2H, H9, H10, J = 16), 7,45 (d, 2H, H7, H8, J = 16), 8.04 (d,
2H, H29, H69, J = 8). C16H14O2, Anal. calc. C: 80.57, H: 5.88, found C:
80.75, H: 5.90.
Animals
Male Wistar-EPM-M1 rats, weighing 130 l 30 g and 230 l 25 g at
the age of seven weeks and four months, respectively, were kept
under controlled conditions (12 h light-dark cycle, 22 l 28C, 60%
air humidity) and had free access to standard laboratory chow
and water. Animals were received from the Central Bioterio of
the University of Vale do Itajaꢀ (Itajaꢀ, Brazil). All animals were
allowed to acclimatize for at least five days prior to the first
treatment. They were fasted for 12 h before experiments and
allowed water ad libitum. All animal procedures were conducted
in accordance with legal requirements relating to the species.
(2E,4E)-1-(29-Hydroxybenzoyl)-4-phenylbutadiene 9
MW = 250 g; m.p.: 118.5–129.28C; yield: 96%; FT-IR (KBr disk,
cm– 1): 1650 (m C=O), 1605 (m C=C); H1-NMR (DMSO-d6, ppm): 6.81
(d, 2H, H3, H5, J = 8), 6.89-7.63 (m, 5H, H39–H69, H2, H4, H6), 7.37
(d, 2H, H9, H10, J = 16), 7.45 (d, 2H, H7, H8, J = 16), 7.88 (d, 1H,
H6'). C15H120, Anal. calc. C: 80.35 H: 5.35, found C: 80.47, H: 5.39.
Acute hypolipidemic activity
An aqueous solution of Triton WR1339 was administered i.p.
(400 mg/kg, body weight, b.w.) to male Wistar rats (230 l 25 g,
n = 6) and after 30 min the compounds investigated (12.5 mmol/
kg, b.w.) or lovastatin (2.5 mmol/kg, b.w.) dissolved in saline solu-
tion, or saline solution (control group) only, was given orally [7,
8]. After 8 h, blood was taken from the occular vein and used for
the determination of serum total cholesterol (TC) and triglycer-
ide (TG) concentrations by enzymatic methods [13, 14]. The con-
centration of VLDL-cholesterol (VLDL-C) in the rats was deter-
mined indirectly by the use of a mathematical formula [10]:
VLDL-C = TG/5.
(2E)-2-(2-Methoxyphenyll)-1-phenylethylene 13
MW = 238 g; m.p.: 59–608C; yield: 94%; FT-IR (KBr disk, cm– 1):
1661 (m C=O), 1601 (m C=C); H1-NMR (DMSO-d6, ppm): 3.91 (s, 3H,
OCH3), 7.06–8.03 (m, 7H, H3–H6, H39–H59), 7.56 (d, 1H, Ha, J =
14), 7.63 (d, 1H, Hb, J = 14), 8.13 (d, 2H, H29, H69, J = 8). C16H14O2,
Anal. calc. C: 80.57, H: 5.88, found C: 80.48, H: 5.92.
(2E,4E)-1-Benzoyl-4-phenylbutadiene 15
MW = 234 g; m.p.: 97–99.58C; yield: 50%; FT-IR (KBr disk, cm– 1):
1656 (m C=O), 1600 (m C=C); H1-NMR (DMSO-d6, ppm): 7.37 (d, 2H,
H39, H59, J = 8), 7.24–7.67 (m, 6H, H2–H6, H49), 7.58 (d, 2H, H9,
H10, J = 14), 7.65 (d, 2H, H7, H8, J = 14), 8.02 (d, 2H, H29, H69, J = 8).
C17H14O, Anal. calc. C: 87.17, H: 5.90, found C: 87.07, H: 5.87.
Chronic hypolipidemic activity
One group of rats (control group, 130 l 30 g, n = 6) was fed on a
hypercaloric-diet (cholesterol 2%, sodium cholate 2%, vitamin
mixture 2%, oligoelements 0.2%, salt mixture 5.8%, corn oil 20%,
cellulose 4%, sucrose 44%, casein 5%, protein 15%) for 30 days
and two groups were fed on a hypercaloric diet plus 0.5 mL of
the compounds investigated (12.5 mmol/kg, b.w., n = 6) or
0.5 mL of lovastatin (2.5 mmol/kg. b.w., n = 6), administered by
oral gavage for the same period [15]. Blood samples for the assays
were collected after the last day of the treatment for the lipid
determinations: TC, high density lipoprotein-cholesterol (HDL-
C), and low density lipoprotein-cholesterol (LDL-C). Rats were
killed and a portion of the liver was removed, homogenized, and
tissue cholesterol was extracted by the Folch method [16] and
analyzed using the cholesterol oxidase method [13]. LDL-C was
estimated using the Friedewald formula [17].
2,3-Dibromo-1,3-bis(4-chlorophenyl)-propan-1-one 16
MW = 437 g; m.p.: 159–1628C; yield: 85%; FT-IR (KBr disk, cm– 1):
1687 (m C=O); H1-NMR (DMSO-d6, ppm): 5.83 (d, 1H, H-8, J = 12),
6.73 (d, 1H, H-7, J = 12), 7.53 8 d, 2H, H3, H5, J = 8), 7.74 (d, 2H,
H39, H59, J = 8), 7.88 (d, 2H, H2, H6, J = 8), 8.31 (d, 2H, H29, H69, J =
8). C15H12OBr2, Anal. calc. C: 48.91, H: 3.26, found C: 48.99, H:
3.31.
2,3-Dibromo-3-(4-methoxyphenyl)-1-phenylpropan-1-one
17
MW = 382 g; m.p.: 140–1448C; yield: 90%; FT-IR (KBr disk, cm– 1):
1685 (m C=O); H1-NMR (DMSO-d6, ppm): 4.74 (s, 3H, OCH3), 5.79 (d,
1H, H-8, J = 12), 6.70 (d, 1H, H-7, J = 12), 7.42–7.98 (m, 7H, H2, H3,
H5, H6, H39-H59), 8.29 (d, 2H, H29, H69, J = 8).C16H14O2Br2, Anal.
calc. C: 48.24, H: 3.51, found C: 48.32, H: 3.57.
References
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2,3-Dibromo-3-(4-nitrophenyl)-1-phenylpropan-1-one 18
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19
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