Synthesis and biological evaluation of gold(III) substituted tetraarylporphyrin chlorides as anticancer reagents

Article abstract of DOI:10.3184/174751911X12992544137142

Substituted gold(III) tetraarylporphyrins have been synthesised. The analogues TPPAuCl (TPP = tetraphenylporhyrin), MeOTPPAuCl, TMOPPAuCl, MeO ₂CTPPAuCl, O₂NTPPAuCl and PyTPPAuCl were evaluated for their in vitro cytotoxic activity a

Full text of DOI:10.3184/174751911X12992544137142

1
90 RESEARCH PAPER
MARCH, 190–194
JOURNAL OF CHEMICAL RESEARCH 2011
Synthesis and biological evaluation of gold(III) substituted
tetraarylporphyrin chlorides as anticancer reagents
a
a
b
b
b
a
Huasheng Chen , Qian Yang , Liang Sun , Zonglei Zhang , Haibo Tong , Aihua Xu and
b
Cunde Wang *
a
School of Medicine, Yangzhou University, 11 Huaihai Road, Yangzhou 225001, Jiangsu, P. R. China
bSchool of Chemistry and Chemical Engineering, Yangzhou University, 180 Siwangting Street, Yangzhou 225009, Jiangsu, P. R. China
Substituted gold(III) tetraarylporphyrins have been synthesised. The analogues TPPAuCl (TPP = tetraphenylporhy-
rin), MeOTPPAuCl, TMOPPAuCl, MeO CTPPAuCl, O NTPPAuCl and PyTPPAuCl were evaluated for their in vitro cyto-
2
2
toxic activity against the Sarcoma 180 mouse tumour cell line panel. Compound MeO CTPPAuCl exhibited good
2
growth inhibitory properties against Sarcoma 180 and afforded IC50 values <3µM for 92.386% of the cell lines in the
panel. Compounds MeOTPPAuCl and TPPAuCl were effective inhibitors of tumour cell growth, but generally less
effective than MeO CTPPAuCl as cytotoxic agents.
2
Keywords: gold (III) substituted porphyrins, tetraaryl porphyrins, in vitro cytotoxicity
Considerable effort has been devoted to the search for new
metal-containing anticancer drugs with preferential anticancer
activity since the introduction of cis-diamminedichloroplatinu
consequence of binding to DNA. The goal is to cause DNA
damage specifically in cancer cells, leading to cell death. It is
known that cisplatin exerts its anticancer effect through prefer-
entially binding to quinine N-7 of cellular DNA. Preliminary
results about the action mechanism of gold(III) complexes
1
,2
37
m(II) (cisplatin) into clinical use. However, although cispla-
tin and its analogues are better anticancer agents so far, the
drug resistance and side effects of these agents still pose major
suggest that gold(III) complexes directly interact with DNA as
3
,4
38,39
problems in their clinical use.
the basis for their cytotoxic effects.
But in vivo and in vitro
Considering that gold(III) possesses the same isoelectronic
binding assays showed that gold(III) porphyrin acted on DNA
noncovalently, which was different to cisplatin. Che and
co-workers’ report showed that gold(III) porphyrin mediated
mitochondrial transmembrane potential depletion, leading to
cytochrome c release, nucleus translocation of apoptosis-
8
configuration (d ) and structural (square planar) characteristics
5
–7
as platinum(II), gold(III) complexes have been important
in developing the field of metal-containing anticancer drug
8
–11
candidates recently.
Some studies showed that gold(III)
30,32
compounds exhibit strong cytotoxic activity in vitro against
inducing factor, and generation of reactive oxygen species.
1
2–15
tumour cells and have tumour-inhibiting properties in vivo.
However, their recent results addressed gold(III) porphyrin-
induced phosphoproteome alterations and modulation of cell
death by the mitogen-activated protein kinase family proteins.
These results suggested that gold(III) porphyrin is a promising
However, it proved difficult to put many available gold(III)
compounds into clinical use because these compounds exhibit
poor solubility or are effective only at relatively high doses.
Moreover, these compounds are usually unstable under physi-
ological conditions, due to the reduction of gold(III) to gold(I).
Based on the above reasons, the design and synthesis of
gold(III) compounds with strongly chelating tetradentate
ligands have been carried out. However, these gold(III) com-
plexes have been found to be inactive towards cancer cells,
presumably due to the over-stabilisation of gold(III) ions
against reduction and demetalation. Messori and co-authors’
report supported the above proposition in which a gold(III)
complex of 1, 4, 8, 11-tetraazacyclotetradecane has poor cyto-
40
anticancer agent directed toward the mitochondria.
Che and co-workers’ studies demonstrated that a gold(III)
modified porphyrin complex (5-hydroxyphenyl-10,15,20-triph
enylporphyrinatogold(III) chloride), with improved aqueous
stability, showed 100- to 3,000-fold higher cytotoxicity than
platinum-based cisplatin and IC50 values in the nanomolar
41
range in a panel of human breast cancer cell lines. Thus the
development of new modified porphyrin ligands chelating to
gold(III) remains an active research area.
We therefore synthesised some new modified porphyrin
ligands with substituted aryl groups to chelate gold(III) for
pharmacological testing, and we compared the efficacy of
these new gold(III) modified porphyrin complexes with that of
cisplatin in suppressing tumour growth.
toxicity towards a series of cancer cells, and has IC values of
5
0
16
>
100 µM. Consequently, a large number of modified tetra-
dentate ligands have been synthesised which give chelate
gold(III) complexes of sufficient stability in the physiological
environment and they have been evaluated for in vitro antican-
cer properties. It has been found that low cisplatin cross resis-
Experimental
1
7–28
tance has been observed in gold complexes.
In particular,
All reagents and solvents were commercial available analytical grade
and used as received except, when necessary, there was further purifi-
cation and drying by standard methods and distillation prior to use.
All evaporation of organic solvents was carried out with a rotary evap-
orator in conjunction with a water aspirator. Melting points were taken
Che and co-workers prepared a series of gold(III) porphyrin
compounds which behave as organic lipophilic cations with a
planar structure, and are stable against demetallation under
physiological conditions. Further in vitro and in vivo studies
revealed that gold(III) porphyrin is a promising anticancer
1
on a hot-plate microscope apparatus and are uncorrected. H NMR
2
9–36
agent for the treatment of colon and liver cancer,
because
spectra were recorded with a Bruker AV-600 spectrometer. IR spectra
were obtained on a Bruker Tensor 27 spectrometer (KBr disc). UV-Vis
spectra were obtained on a UV 2501 PC spectrometer. The MS spectra
were obtained on a ZAB-HS mass spectrometer with 70 eV. 5, 10, 15,
the porphyrin ligand in these compounds can greatly stabilise
the gold(III) centre, drastically reduce its redox reactivity and
oxidising character, and carry the metal to the cellular targets.
The use of gold(III) porphyrin complexes may provide an
advantage for clinical application.
Researches on the mechanism of action of metal complexes
indicate that the cytotoxic effects of metal complexes are the
2
0-tetraaryl porphyrins (1–3) were synthesised by the reported
42,43
method.
Elemental analytical data were obtained using a model
2
40 elementary instrument. Mycoplasma-free newborn calf serum
was purchased from Hangzhou Sijiqing Biological Engineering
Materials Co., Ltd. Cisplatin (Cis) was the product of Jiangsu Hansen
Pharmaceutical Co., Ltd. RPMI 1640, MTT and DMSO were
purchased from Sigma-Aldrich Chemical Co.
*
Correspondent. E-mail: wangcd@yzu.edu.cn

JOURNAL OF CHEMICAL RESEARCH 2011 191
1
Sarcoma 180 mouse tumour cell line (S180) was purchased from
Shanghai Institute of Cell Biology, Chinese Academy of Science.
The cell line was cultured in RPMI 1640 medium with 10% newborn
calf serum serum. It was maintained in a humidified incubator with
5-Pyrdinyl-10,15,20-triphenylporphyrin (6): M.p. > 250 °C;
NMR (CDCl
7.80 (m, 9H, Ph-CH
Hz, 6H, Ph-CH , 8.79 (d, J = 4.2 Hz, 2H, Ph-CH
Por-CH , 9.03 (s, 2H, Por-CH ; IR (KBr): υ 3446(s), 1634(w), 1590(w),
1473(w), 1396(w), 1351(w), 1070(w), 970(w), 798(m), 710(m),
H
, 600 MHz), δ (ppm): –2.82 (s, 2H, inner-NH), 7.75–
, 8.17 (d, J = 5.4 Hz, 2H, Ph-CH), 8.21 (d, J = 6.6
, 8.86–8.90 (m, 6H,
3
)
)
)
an atmosphere of 95% air and 5% CO at 37 °C. The cells were con-
)
)
2
tinuously passaged once every 3–4 days. Growing cells were collected
for experiments.
−1
657(w) cm ; UV-Vis(CH
Cl )/nm 416, 513, 548, 586, 644. Calcd for
C H N : C, 83.88; H, 4.75; N, 11.37. Found: C, 83.62; H, 4.61;
2
2
43
29
5
Preparation 5,10,15-triphenyl-20-substitutedphenyl porphyrins 4–6
A mixture of benzaldehyde (3.18 g, 30.0 mmol), substituted aromatic
aldehyde (10.0 mmol) and freshly distilled pyrrole (2.68 g, 40.0
mmol) in propionic acid (140 mL) was refluxed for 3 h. After comple-
tion of the reaction was checked by TLC, the mixture was cooled in
an ice-water bath, the crude product filtered and the filter cake was
washed thoroughly with methanol (100 mL) then dichloromethane
N, 11.26%.
Preparation gold(III) substituted porphyrins 7–12
A mixture of substituted porphyrin 1–6 (2.5 mmol), K[AuCl ] (2.82 g,
4
7
.5 mmol) and sodium acetate (2.05 g, 25 mmol) in acetic acid (5 mL)
was refluxed for 3 h. After completion of the reaction was checked by
TLC, the crude product was obtained by removing acetic acid. Next
the solid product was washed thoroughly with dichloromethane then
water. The crude product then was purified by column chromato-
graphy (silica gel, DCM/methanol: 5/1 V/V). The purified product
was dissolved in acetone, and after filtering the mixture solution was
treated with LiCl in aqueous acetone. Analytically pure gold(III) por-
phyrin compounds 7–12 were obtained as chloride salts in 76–85%
yields.
(10 mL). The resulting purple crystals were air dried, the crude
product was purified by column chromatography (silica gel, DCM/
n-hexane: 1/5 V/V), and recrystallisation from ethanol gave pure
products 4–6.
5
-(p-Methoxycarbonylphenyl)-10,15,20-triphenyl porphyrin (4):
1
M.p. > 250 °C; H NMR (CDCl , 600 MHz), δ (ppm): –2.79 (s, 2H,
inner-NH), 4.11 (s, 3H, –COOCH ), 7.74–7.79 (m, 9H, Ph-CH), 8.21
3
3
5
,10,15,20-tetraphenylporphyrinato gold(III) chloride (7): M.p.
(
(
d, J = 6.6 Hz, 6H, Ph-CH), 8.31 (d, J = 7.8 Hz, 2H, Ph-CH), 8.44
d, J = 7.8Hz, 2H, Ph-CH), 8.79 (d, J = 4.2 Hz, 2H, Por-CH), 8.85 (s,
1
1
8
8
2
7
78–180 °C; H NMR (600 MHz, CDCl ), δ (ppm): 7.86 (d, J = 7.2Hz,
3
H, Ph-CH), 7.89 (d, J = 7.2Hz, 4H, Ph-CH), 8.26 (d, J = 7.8Hz,
H, Ph-CH , 9.26 (s, 8H, Por-CH . IR (KBr): υ 3428(s), 2924(w),
6
1
1
H, Por-CH ; IR (KBr): υ 3442(s), 3319(w), 2924(w), 2853(w),
)
)
)
812(m), 1722(s), 1604(w), 1472(w), 1437(w), 1394(w), 1353(w),
858(w), 1630(w), 1448(w), 1368(w), 1080(w), 1029(w), 803(w),
−1
279(s), 1182(w), 1106(w), 800(m), 739(w) cm ; UV-Vis(CH Cl )/
−1
2
2
57(w), 704(w) cm ; UV-Vis (CH Cl )/nm 408, 520; MS: 809.6
2
2
nm 416, 513, 548, 589, 646. Anal. Calcd for C H N O : C, 82.12; H,
−
46
32
4
2
(
M+1-Cl , 100%). Anal. Calcd for C H N ClAu: C, 62.53; H, 3.34;
44 28 4
4
.79; N, 8.33. Found: C, 82.04; H, 4.50; N, 8.62%.
-(p-Nitrophenyl)-10,15,20-triphenyl porphyrin (5): M.p. > 250 °C;
H NMR (CDCl , 600 MHz), δ (ppm): –2.79 (s, 2H, inner-NH),
N, 6.63. Found: C, 62.48; H, 3.50; N, 6.68%.
-p-Methoxyphenyl-10,15,20-triphenylporphyrinatogold(III) chlo-
5
5
1
1
3
ride (8): M.p. 156–158 °C; H NMR (600 MHz, CDCl ), δ (ppm):
3
7
.75–7.81 (m, 9H, Ph-CH , 8.21 (d, J = 7.2Hz, 6H, Ph-CH), 8.40
)
4.13 (s, 3H), 7.40 (d, J = 8.4Hz, 2H), 7.86–7.92 (m, 9H), 8.16 (d,
J = 8.4 Hz, 2H), 8.24 (d, J = 8.4 Hz, 6H), 9.28 (d, J = 7.2 Hz, 6H),
9.34 (d, J = 5.4 Hz, 2H); IR (KBr): υ 2922 (s), 2856 (w), 1737 (w),
1612 (w), 1453 (w), 1368 (w), 1251 (w), 1176 (w), 1081 (w), 1027
(w), 806 (w), 756 (w), 705 (w) cm ; UV-Vis (CH Cl )/nm 408, 520;
MS: 839.9 (M+1-Cl , 100%). Anal. Calcd for C H N OClAu:
(
d, J = 8.4Hz, 2H, Ph-CH , 8.64 (d, J = 8.4Hz, 2H, Ph-CH , 8.74
)
)
(
d, J = 4.2Hz, 2H, Por-CH), 8.86–8.90 (m, 6H, Por-CH ; IR (KBr):
)
υ 3446(s), 2918(w), 2850(w), 1596(w), 1517(w), 1472(w), 1392(w),
−
1
−1
1
345(m), 1073(w), 840(w), 798(m), 706(m) cm ; UV-Vis(CH Cl )/
2
2
2
2
−
nm 418, 514, 549, 588, 645; Anal. Calcd for C H N O : C, 80.10;
44
29
5
2
45 30 4
H, 4.43; N, 10.62. Found: C, 80.02; H, 4.68; N, 10.49%.
C, 61.76; H, 3.46; N, 6.40. Found: C, 61.50; H, 3.58; N, 6.53%.
Scheme 1 Preparation of substituted porphyrin ligands 1–6.
Scheme 2 Preparation of gold(III) substituted porphyrin ligands.

1
92 JOURNAL OF CHEMICAL RESEARCH 2011
Table 1 Preparation of substituted porphyrins (1-6) and
gold(III) porphyrins (7–12)
1357(w), 1242(m), 1176(w), 1079(w), 1026(m), 802(w), 756(w),
1
−
−
702(w) cm ; UV-Vis(CH Cl )/nm 410, 521; MS: 868.1 (M+1-Cl ,
2
2
1
00%). Anal. Calcd for C H N O ClAu: C, 61.17; H, 3.35; N, 6.20.
46 30 4 2
Entry R′
R″
X
Ligands
Au (III) complexes
(yield/%)
Found: C, 61.32; H, 3.60; N, 6.36%.
-(p-Nitrophenyl)-10,15,20-triphenylporphyrinatogold(III) chloride
(
yield/%)
5
1
(
11): M.p. >250 °C; H NMR (CDCl , 600 MHz), δ (ppm): 7.78–7.82
1
2
3
4
5
6
H
H
OCH
CO
CO
NO
C
C
C
C
C
N
23.0 (1)
8.8 (2)
22.0 (3)
9.0 (4)
8.5 (5)
6.5 (6)
78.0 (7)
95.5 (8)
65.5 (9)
83.0 (10)
40.2 (11)
82.0 (12)
3
H
3
(m, 9H, Ph-CH), 8.18 (s, 6H, Ph-CH), 8.47 (s, 2H, Ph-CH), 8.65 (s,
2H, Ph-CH), 9.06 (s, 2H, Ph-CH), 9.18 (d, J = 8.4 Hz, 6H, Por-CH);
IR (KBr): υ 3438(s), 2922(m), 2856(w), 1733(w), 1629(w), 1517(w),
CO
H
H
H
2
CH
3
2
CH
CH
3
3
2
−
1
2
1452(w), 1346(w), 1086(w), 1028(w), 803(w), 756(w), 703(w) cm ;
UV-Vis(CH Cl )/nm 408, 520; MS: 855.1 (M+1-Cl , 100%). Anal.
−
2
2
Calcd for C H N O ClAu: C, 59.37; H, 3.06; N, 7.87. Found:
44
27
5
2
C, 59.22; H, 3.02; N, 7.92%.
-pyridinyl-10,15,20-triphenylporphyrinato gold(III) chloride (12):
5
1
5
,10,15,20-tetra-p-methoxycarbonylphenylporphyrinatogold(III)
M.p. > 250 °C; H NMR (CDCl , 600 MHz), δ (ppm): 7.84–7.91 (m,
3
1
chloride (9): M.p. >250 °C; H NMR (600 MHz, CDCl ), δ (ppm):
.13 (s, 12H, –COOCH ), 8.36 (d, J = 7.8 Hz, 8H, Ph-CH), 8.52
d, J = 7.8 Hz, 8H, Ph-CH), 9.18 (s, 8H, Por-CH ; IR (KBr): υ 3433(m),
923(m), 2856(w), 1717(s), 1609(w), 1436(w), 1278(s), 1185(w),
9H, Ph-CH), 8.25 (d, J = 7.8 Hz, 8H, Ph-CH), 9.14 (d, J = 4.2 Hz, 2H,
Ph-CH), 9.18 (d, J = 5.4 Hz, 2H, Por-CH), 9.26 (s, 4H, Por-CH), 9.29
(s, 2H, Por-CH); IR (KBr): υ 3437(s), 2925(m), 2859(w), 1629(w),
3
4
(
2
1
3
)
−
1
1447(w), 1368(w), 1083(w), 1031(w), 804(w), 759(w), 706(w) cm ;
−
1
−
107(m), 1024(m), 808(w), 762(w), 708(w) cm ; UV-Vis(CH Cl )/
UV-Vis(CH Cl )/nm 407, 519; MS: 811.2 (M+1-Cl , 100%). Anal.
2
2
2
2
−
nm 408, 519; MS: 1041.8 (M+1-Cl , 100%). Anal. Calcd for
C H N O ClAu: C, 57.98; H, 3.37; N, 5.20. Found: C, 57.80; H,
Calcd for C H N ClAu: C, 61.04; H, 3.22; N, 8.28. Found: C, 61.24;
43 27 5
5
2
36
4
8
H, 3.18; N, 8.52%.
3
.26; N, 5.46%.
-(p-Methoxycarbonylphenyl)-10,15,20-triphenylporphyrinatogol
Cytotoxicity assay for gold(III) substituted tetraarylporphyrin chlo-
rides of the effect on S180 cell proliferation: Gold(III) substituted
tetraarylporphyrin chlorides were prepared at the concentrations
5
1
d(III) chloride (10): M.p. >250 °C; H NMR (CDCl , 600 MHz),
δ (ppm): 4.13 (s, 3H, –COOCH ), 7.82–7.88 (m, 9H, Ph-CH , 8.30 (s,
6
Ph-CH , 9.19 (s, 2H, Por-CH , 9.26–9.27 (m, 6H, Por-CH); IR (KBr):
υ = 3414(w), 2921(s), 2852(m), 1737(w), 1601(w), 1498(w), 1460(w),
3
−
5
−1
−5
−1
−5
−1
−6
−1
3
)
6.4×10 mol L , 3.2×10 mol L , 1.6×10 mol L , 8×10 mol L ,
−
6
−1
−6
−1
H, Ph-CH), 8.42 (d, J = 8.4 Hz, 2H, Ph-CH , 8.51 (d, J = 7.2 Hz, 2H,
4×10 mol L and 2×10 mol L respectively. DMSO was used as
latent solvent with the highest concentration less than 0.1% in solution
of tetraarylporphyrin. The control groups of cisplatin, blank (1640)
)
)
)
Table 2 Cytotoxicity of gold(III) substituted tetra-arylporphyrin chloride against Sarcoma 180 mouse tumour cell line in vitro
1
IC50 /µmol L−1
Number
1
Symbol
Compound
TPPAuCl
Dose/µmol L−
Inhibition rate/%
7
32
79.375
62.344
43.594
27.344
12.031
5.313
74.112
78.934
61.168
45.178
27.284
15.863
25.781
31.875
15.469
12.188
11.719
2.031
79.569
92.386
88.579
50.888
32.487
31.218
37.281
23.197
17.398
2.632
10.021
16
8
4
2
1
2
3
4
5
6
7
8
9
TPPOCH
3
AuCl
32
5.571
133.613
2.820
16
8
4
2
1
TMOPPAuCl
32
16
8
4
2
1
10
11
12
/
3
TPPCOOCH AuCl
32
16
8
4
2
1
2
TPPNO AuCl
32
44.133
27.683
16.453
16
8
4
2
1
0.292
0.000
TPPPyAuCl
Cisplatin
32
53.412
43.763
25.480
16.045
11.354
6.557
60.501
46.802
39.789
28.998
23.617
7.411
16
8
4
2
1
32
16
8
4
2
1

JOURNAL OF CHEMICAL RESEARCH 2011 193
Fig. 1 Inhibition rate of gold(III) substituted tetra-aryl porphyrin chloride against Sarcoma 180 mouse tumour cell line in vitro.
Fig. 2 IC50 of gold(III) substituted tetra-aryl porphyrin chloride against Sarcoma 180 mouse tumour cell line in vitro.
and DMSO solvent were set up at the same time. The cytotoxicity of
gold(III) substituted tetraarylporphyrin chlorides was determined by
The configuration change of the S180 cells was observed under the
microscope. After the cells were seeded in 96-well plates, light, round
and dense cells could be seen under the microscope. Drug effects were
observed after 44h, showing that cells were significantly reduced from
circular into spindle.
44
MTT cytotoxic assay. S180 cells were plated in 96-well plates at
5
1
×10 /mL and 100 µL/well in complete media. Then the prepared and
various amounts of gold(III) substituted-tetraarylporphyrin chloride
and cisplatin were plated in 96-well plates containing S180 cells
and incubated commonly for 44 h. 100 μL of supernatant liquid was
The anti-tumour effect of gold(III) substituted tetraarylporphyrin
chloride: The results showed that compound 7, 8 and 9 (1–32 µmol
−
1
−1
sucked from each hole, 10 µL of MTT (5 mg mL ) was added in and
cultured for 4h; the media was then removed and hydrochloric acid/
isopropanol at 100 µL/well was added. After spurging for 5 minutes
using the micro oscillator to dissolve the MTT crystal, the OD value
was measured at 570nm using a Model Elx 800 Autoplate reader
L ) exert a significant inhibitory effect on the growth of S180 cells,
and compound 10 displays more prominent activity than lead com-
pound 7 and cisplatin. Compounds 9, 11 and 12 have a weaker inhibi-
−
1
tory effect on S180 cells, IC50 values were more than 10 µ mol L ,
−
1
while IC50 values of 8 and 10 were less than 10 µmol L . (Table 2,
(Bio-Tek Instruments, USA).
Figs 1 and 2)
All the experimental data were compiled and analysed according to
SPSS 15.0 software. Data were expressed as the mean ± SD.
These results indicate that the gold atom located in the centre of the
porphyrin ring has a major impact on the effect of the whole com-
pound. If this atom were substituted by other metal atom such as
−
1
copper (copper(II) tetraphenylporphyrin: IC (µmol L ) > 200), the
50
Results and discussion
anti-tumour activity in vitro would decrease notably. The gold(III)
substituted porphyrin with methoxycarbonyl- or methoxy-
Schemes 1 and 2 show the synthetic routes to the target gold(III) sub-
stituted- tetraarylporphyrin in both the mono-substitutent and four-
substituent series. Using reaction conditions similar to those reported
a
substituted group has greater anti- cancer activity than the lead com-
pound TPPAuCl, which has potential for anti-tumour drugs. Thus,
42,43
previously,
the substituted porphyrin ligands 1–6 were prepared
the gold(III) substituted porphyrin MeO CTPPAuCl is regarded as
2
from the appropriate aromatic aldehydes and pyrrole (Scheme 1) in
yield 6.5–23%. Gold(III) porphyrin compounds were synthesised by
a useful lead compound for further structural optimisation, the
anti-tumour mechanism of which will be studied in the future.
the treatment of K[AuCl ] with the porphyrin ligand in the presence of
4
NaOAc in acetic acid. After purification by column chromatography
and metathesis reaction with LiCl in aqueous acetone, the gold(III)
porphyrin compounds were obtained as chloride salts in 40.2–95.5%
yields.
Financial support of this research by National Natural Science
Foundation of China (NNSFC 20872125) is gratefully
acknowledged by authors.

1
94 JOURNAL OF CHEMICAL RESEARCH 2011
2
2
G. Marcon, S. Carotti, M. Coronnello, L. Messori, E. Mini, P. Orioli,
T. Mazzei, M.A. Cinellu and G. Minghetti, J. Med. Chem., 2002, 45,
Received 29 November 2010; accepted 2 March 2011
Paper 1000452 doi: 10.3184/174751911X12992544137142
Published online: 23 March 2011
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2
2
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