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Ga-Pentixafor
FrancescaRusso, MassimoMenichini, MariaRicci,
LauraTravascio, HabibollahDadgar, HosseinArabi,
NasimNorouzbeigi, MariaSilviaDe Feo,
HabibZaidi, BatoolAlbalooshi, andAndreaCimini
17
Abbreviations
CT Computed tomography
CXCL12 C-X-C motif chemokine 12
CXCR4 Chemokine receptor 4
DOTA 1,4,7,10-tetraazacyclododecane1,
4,7,10-tetraacetic acid
FDG Fluorodeoxyglucose
FWHM Full width at half maximum
The authors declare they have obtained permission for any
previously published material used in their chapter.
F. Russo
Nuclear Medicine Unit, Clinica Ars Medica, Rome,
Italy
M. Menichini · A. Cimini (*)
Nuclear Medicine Unit, St. Salvatore Hospital,
L’Aquila, Italy
M. Ricci
Nuclear Medicine Unit, Cardarelli Hospital,
Campobasso, Italy
L. Travascio
UOC Nuclear Medicine, P.O.Pescara Santo Spirito,
Pescara, Italy
H. Dadgar · N. Norouzbeigi
Razavi Cancer Research Center,
Imam Reza International University, Razavi Hospital,
Mashhad, Iran
H. Arabi
Division of Nuclear Medicine and Molecular
Imaging, Geneva University Hospital, Geneva,
Switzerland
Hossein.Arabi@unige.ch
e-mail:
MR Magnetic resonance
NET Neuroendocrine tumor
OSEM Ordered-subsets expectation
maximization
PET Positron emission tomography
PET/CT Positron emission computed tomog-
raphy/computed tomography
PET/MR Positron emission computed tomog-
raphy/magnetic resonance
M. S. De Feo
Department of Radiological Sciences, Oncology and
Anatomo-Pathology, Sapienza, University of Rome,
Rome, Italy
mariasilvia.defeo@uniroma1.it
e-mail:
H. Zaidi
Division of Nuclear Medicine and Molecular
Imaging, Geneva University Hospital, Geneva,
Switzerland
Geneva University Neurocenter, Geneva University,
Geneva, Switzerland
Department of Nuclear Medicine and Molecular
Imaging, University of Groningen, University
Medical Center Groningen, Groningen, Netherlands
Department of Nuclear Medicine, University of
Southern Denmark, Odense, Denmark
Habib.Zaidi@unige.ch
e-mail:
B. Albalooshi
Dubai Nuclear Medicine & Molecular Imaging Center,
Dubai Academic Health Corporation, Dubai, UAE
bealbalooshi@dha.gov.ae
e-mail:
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
F. Calabria, O. Schillaci (eds.), Radiopharmaceuticals,
https://doi.org/10.1007/978-3-031-54196-4_17
287
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F. Russo et al.
PET/MRI Positron emission computed tomog-
raphy/magnetic resonance imaging
SUVmax Maximum standardized uptake
value
TME Tumor microenvironment
17.1 Synthesis
The synthesis of 68Ga-DOTA-Pentixafor is
mostly performed using a specic, fully automated module (Scintomics GRP®,
Fuerstenfeldbruck, Germany). The module is
controlled by a computerized system which runs
the valves and syringes on the cassettes (specic
for the synthesis of [68Ga]-DOTA-Pentixafor)
obtained from ABX pharmaceuticals (ABX,
Advanced Biochemical Compounds, Radeberg,
Germany). The system is used to produce other
radiopharmaceuticals, such as 68Ga-prostate specic membrane antigen (68Ga-PSMA),
68
Ga-DOTA0-Tyr3octreotide (68Ga-DOTATOC),
68
Ga-DOTA0-Tyr3octreotate (68Ga-DOTATATE),
using a specic synthesis cassette. For each specic radiopharmaceutical process, there is a specic template computer program [1].
In German experience, the germanium-68
(68Ge)/68Ga generators used is a good manufacturing practice compliant generator with
1.85 GBq total activity [1]. Elution is performed on the rst day of the week and on nonsynthesis days: the build-up of metal ions on
the column must be eluted on a daily basis and
within 24h prior to any
68
Ga-DOTA-Pentixafor
synthesis. Elution process is performed using a
0.1 M HCl solution in approximately 5 min.
The elution volume is 10 mL. Synthesis of
68
Ga-DOTA-Pentixafor is performed using
10μg of peptide [1].
17.2 Pharmacokinetics
68
Ga-Pentixafor is a PET radiopharmaceutical
that binds chemokine receptor CXCR4, overexpressed in a variety of malignancies [2].
Tumor microenvironment (TME) is a network
of extracellular matrix, stromal cells, and
immune cells working together to create a
favorable home for tumor cells. The stromal
component of the TME includes different cell
types, such as cancer- associated broblasts,
platelets, and immune cells [2–7]. CXCR4 is a
small, secreted chemokine receptor with a
seven-transmembrane structure with seven
helical regions connected by six extra-membrane loops. Being above all expressed in B
lymphocytes and plasmacytoid dendritic cells,
it potentially promotes an immunosuppressive
state contributing to tumor progression.
Moreover, CXCR4 and its ligand stromal cell
derived factor-1 (SDF-1, also known as
CXCL12) play a key role in various physiologic processes based on both recruitment and
homing of stem cells, progenitor cells, and
immune cells. It is thus important in embryogenesis, neo- angiogenesis, hematopoiesis, and
inammation [2–9].
The binding of CXCL12 to CXCR4 induces
vascular permeability and allows tumor cell
extravasation, thus promoting the metastatic process in several organs including lung, liver, skeletal muscle, brain, kidney, heart, skin, and bone
marrow [10, 11]. Moreover, the activation of
CXCR4 also promotes vasculogenesis and
hypoxia-driven angiogenesis by recruiting
CXCR4- positive pro-angiogenic cells, which
contribute to the spread of cancer cells. In addition, the CXCL12/CXCR4 axis enhances vascular permeability and enables tumor cell
extravasation, all ultimately promoting the metastatic process [
2–11].
17.3 Physiological Distribution
Sites of signicant 68Ga-Pentixafor uptake
include spleen, kidneys, bone marrow, heart, and
liver [4, 12].
An initial high uptake is observed in the
liver, corresponding to a value of 5.6% of
injected activity after 4min, and is followed
by a rapid washout to 0.2% after 4 h [4].
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289
Significant tracer uptake is also observed in
the heart with 3.1% after 4min, declining to
less than 0.1% after 4h. Being characterized
by low uptake compared with other visible
organs, the gallbladder shows favorable imaging characteristics, with high tumor-to-background (TBR) ratios 30min after intravenous
injection [4].
The highest absorbed dose per unit activity is
observed in the urinary bladder wall (8.14E–
02mGy/MBq), followed by the spleen (5.38E–
02mGy/MBq) and the kidneys (3.5E–02 mGy/
MBq). Organ-absorbed doses associated with
68
Ga-Pentixafor are lower than those of other
PET radiopharmaceuticals [12].
17.4 Clinical Indications
CXCR4 is overexpressed on tumor cell surface
of more than 30 different human cancers
including both solid and hematological malignancies, thereby rendering this G-protein coupled receptor an attractive target for imaging
and therapy. As previously reported, CXCR4
promotes tumor growth, metastatic process,
angiogenesis and tumor–cell interaction, and
its expression is associated with more aggressive tumor behavior and poorer prognosis [2].
In addition, the CXCR4–CXCL12 axis is
implicated in treatment resistance by providing a safe space for tumor cells in the bone
marrow which makes cancers resistant to chemotherapy. Therefore, the inhibition of the
CXCR4 axis would be the goal of oncological
therapies by slowing disease progression,
inhibiting metastatic process and improving
tumor chemosensitivity. As
assays CXCR4 expression in vivo, it represents a predictive biomarker for CXCR4targeting treatments and a valuable
theragnostic agent to select patients likely to
benefit from targeted radionuclides therapies
[3]. In fact, although 68Ga-Pentixafor-based
imaging currently plays a complimentary role
to 18F-FDG PET in the staging of solid tumors,
68
Ga-pentixafor
it may provide important prognostic information and aid in the selection of patients eligible
for CXCR4-targeting therapies and in treatment response evaluation [
68
Ga-Pentixafor PET aims to discover a new
2]. In this scenario,
theragnostic marker rather than establish
another diagnostic tracer [2].
In high grade head and neck squamous carcinoma, the overexpression of CXCR4 was
revealed in recent studies. Chen et al. demonstrated low tracer uptake with a TBR of less than
4, with only mild tracer accumulation on the
68
Ga-Pentixafor PET [2, 13], as imaging with a
CXCR4-targeting tracers generally results in
lower SUVmax values and lower TBR when
compared to 18F-FDG PET.
On the contrary, in patients with glioblas-
toma, tumor detection is increased in PET with
68
Ga-Pentixafor compared to 18F-FDG, because
of the absence of physiological brain uptake
[14]. In these subjects, the expression CXCR4-
CXCL12 relates with World Health Organization
(WHO) tumor grade, and it is associated with
necrosis/angiogenesis and therefore more inltrative phenotypes. Although CXCR4 mRNA
expression appears to be highest in glioblastomas, there is a large variation of CXCR4 expression in glioblastoma tissue itself, both within
and between tumors. When high CXCR4 expression is present, targeted imaging with
68
Ga-Pentixafor might complement tumor imaging. In this context, both tumor imaging and targeted radionuclide therapy might improve
survival rates of a part of patients showing
CXCR4 expression [
14].
In esophageal cancer (OC), Kai etal. demonstrated CXCR4 protein expression in 75 (55%) of
136 esophageal tumors [5], and CXCR4 expression was associated with a poor clinical outcome
with a median overall survival of 20 months in
patients with CXCR4-positive tumors vs
76months for CXCR4-negative tumors. This was
conrmed by Goto et al. [6], who showed how
75.6% of the 172 OC specimens stained positive
for CXCR4 signicantly correlated with clinical
distant metastasis, pathological lymph node
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F. Russo et al.
metastasis, and vascular invasion. Furthermore,
Yang et al. demonstrated high expression of
CXCR4 in 101 patients with esophageal squamous cell carcinoma versus absence of uptake in
normal tissues [15]. Many studies comparing
68
Ga-Pentixafor and 18F-FDG revealed the latter
as a more sensitive method, but Linde etal. studying 10 patients with OC revealed 53% of lesions
positive on both tracers, while 19% of lesions
were 18F-FDG positive and Pentixafor negative.
Interestingly, 68Ga-Pentixafor revealed more sites
of disease than 18F-FDG, specically 7/26 (27%)
of 18F-FDG negative lesions were 68Ga-Pentixafor
positive [16].
68
Ga-Pentixafor nds application in G3 neuroendocrine tumors (NETs), which are keeping
higher CXCR4 expression than G1 or G2 NETs,
for which 68Ga-DOTATOC remains the most sensitive tracer [2, 17].
Emerging research shows that small cell lung
cancer (SCLC) expresses CXCR4 invitro, and
CXCR4 expression has been investigated to
assess if these patients could benet from target
therapy. Kaemmerer et al. evaluated 34 SCLC
samples by immunohistochemistry. In their
study CXCR4, predominantly localized at the
plasma membrane of the tumor cells, was correlated with clinical data and overall patient survival [18].
Pollino etal. assessed CXCR4 expression in
48 primary osteosarcoma samples compared to
10 healthy bone samples and demonstrated that
in osteosarcoma, CXCR4 expression was directly
correlated to both the histological grade of the
tumor and its aggressiveness. Thus far, this tracer
may have a role in prognostic assessment and in
selecting patients who may benet from therapies targeting CXCR4 [
2, 19].
Shiozaki et al. showed high CXCR4 expression in gynecological malignancies in vitro. Its
expression positively correlated with more
aggressive disease, lymph nodal dissemination,
and metastatic disease [2].
As concerning breast cancer (BC), the overexpression of CXCR4 on immunohistochemistry
has shown to be associated with poorer prognosis. A meta-analysis by Zhang etal. including 13
eligible studies consisting of 3865 participants
showed that CXCR4 overexpression was associated with lymph node inltration, distant metastasis, and signicantly reduced disease-free
survival (DFS) and overall survival (OS) [
2]. This
was conrmed in a meta-analysis of 15 studies by
Xu et al., which included 3104 patients, and
showed that OS and DFS were lower in BC
patients with high levels of CXCR4 expression.
The comparison between 68Ga-Pentixafor and
18
F-FDG revealed inferiority of the former in the
detection of metastatic lesions and lower
SUVmax values [20].
Even in prostate cancer CXCR4 expression is
signicantly associated with a more aggressive
disease, the presence of metastasis, and poorer
cancer specic survival [2].
68
Ga-Pentixafor PET is also useful in adrenocortical carcinoma. Chifu et al. evaluated the
invitro expression of CXCR4in 18 tumor samples and found a strong membrane expression of
CXCR4, which related with Ki-67 index [21].
In primary colon cancer, Ottaiano etal. demonstrated a correlation between CXCR4 expression and response to rst line chemotherapy, but
68
Ga-Pentixafor PET was inferior to 18F-FDG
PET [2, 22], indicating therefore that
68
Ga-Pentixafor PET cannot replace but remains
complementary to
18
F-FDG PET.
CXCR4 is overexpressed in 88.33% (65/78)
of hepatocellular carcinoma and plays a signicant role in the metastatic process by promoting
the migration of tumor cells [2].
Particular attention should be paid to
patients with melanoma, where invivo CXCR4
overexpression has been reported and has been
found to be higher in metastasis than primary
tumors and also associated with a higher tumor
stage. In a meta-analysis of 13 studies investi-
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291
gating CXCR4 expression in the tumor samples of 656 patients with malignant melanoma,
it was found that the high expression of CXCR4
is associated with ulceration, increased tumor
thickness, and lymph node metastasis [23]. Vag
etal. compared 68Ga-Pentixafor with 18F-FDG
in a heterogenous group of patients of whom
two had malignant melanoma. In these subjects
68
Ga-Pentixafor detected all the four metastatic
lesions, as did 18F- FDG PET, even if the
SUVmax was slightly higher on 18F-FDG PET
[20].
In a meta-analysis of 14 studies involving
1203 participants and performed by Si etal., the
authors showed that CXCR4 expression is signicantly higher in patients with metastatic renal
carcinoma than in patients with non-metastatic
disease, and that its expression is signicantly
associated with poorer prognosis [24].
As regards onco-hematological diseases, the
role of 68Ga-pentixafor PET in lymphoproliferative disorders is not well dened. Interesting
results were shown in a study by Haug et al.,
evaluating 36 patients with diagnosis of mucosaassociated lymphoid tissue (MALT) lymphoma.
In 33 patients, MALT lymphoma showed high
uptake of the tracer, suggesting a potential role of
68
Ga-Pentixafor PET in the disease assessment of
such patients [25]. Moreover, as described by
Albano et al., 68Ga-Pentixafor PET may be an
interesting imaging technique for the evaluation
of marginal zone lymphoma, central nervous system lymphoma, and lymphoplasmacytic lymphoma as well [
26].
As CXCR4 is overexpressed in myeloma
multiple cells [27], 68Ga-Pentixafor PET has
shown promising results in the diagnosis of this
disease. In a study by Pan etal., evaluating 30
patients with newly diagnosed myeloma multiple, 68Ga-pentixafor PET/CT presented a higher
positive rate than 18F-FDG PET/CT in the
detection of malignant lesions (93.3% vs.
53.3%) [27]. Furthermore, promising results
have been reported in a recent study by
Shekhawat and collaborators, evaluating 34
patients with treatment naive multiple myeloma
and showing how in comparison to 18F-FDG
PET/CT, 68Ga-Pentixafor PET/CT presented
higher disease extent in the majority of patients
(68%) [28].
17.5 Clinical Cases
See Figs.17.1, 17.2 and 17.3.
Fig. 17.1 Maximum intensity projection (MIP) image of
whole-body
showing accumulation of the radiotracer in kidneys, urinary bladder, spleen, nasopharynx, and moderate inhomogeneous uptake in the entire axial skeleton
68
Ga-Pentixafor PET in a healthy volunteer,
292
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F. Russo et al.
Fig. 17.2 33-year-old male with diagnosis of glioblastoma: axial CT (a), 68Ga-Pentixafor PET/CT (b) and PET (c, d)
images show a left occipito-parietal lesion with SUVmax 2.68
ab
cd
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293
e
Fig. 17.3 58-year-old female diagnosed by glioblastoma: axial CT (a),
(c, d) images show a left intra-axial para-falcine mass
68
Ga-Pentixafor PET/CT (b) and PET
f
with extension to contralateral hemisphere: the highest
SUVmax of the lesion was 3.01. The lesion is also
depicted in T2W FLAIR (e) and T1W (f) MRI images
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F. Russo et al.
17.6 PET/CT Acquisition Protocols
As we reported before, 68Ga-Pentixafor PET
imaging has been used for the evaluation of
malignancies with high CXCR4 expressions.
Since 68Ga-Pentixafor PET scanning is performed
for a variety of indications, different acquisition
protocols are followed in 68Ga-Pentixafor studies.
No specic dietary preparation is needed in
68
Ga-Pentixafor PET examinations since the glu-
cose metabolic path is not involved in
68
Ga-Pentixafor uptake (as opposed to 6h fasting
required in 18F-FDG PET) [29].
In brain 68Ga-Pentixafor examinations, either
hybrid PET/MR or PET/CT scanners are
employed to perform PET scans in one- or twobed positions [30]. A typical intravenous activity
of 1.5MBq/kg is administered in brain studies,
leading to injected activities ranging from 80 to
170 MBq per scan/patient [13, 31, 32].
68
Ga-Pentixafor PET examinations are typically
conducted 60min post-injection to ensure a highlevel uptake in the target regions. Brain
68
Ga-Pentixafor PET scans are normally performed 30–60min post-injection, depending on
the centers/acquisition protocols [33]. Brain PET
scan duration varies across centers ranging from
10 to 30min (typically 20min), wherein a single
bed position with an acquisition time of 10min is
conducted for glioblastoma tissue analysis on a
Biograph mCT hybrid PET/CT scanner (Siemens
Healthineers) [14] and an acquisition time of
30min is applied for central nervous system lymphoma assessment using the Biograph mMR
hybrid PET/MR scanner (Siemens Healthineers)
[
33].
For attenuation and scatter correction, a lowdose CT scan is commonly performed on hybrid
PET/CT scanners. The low-dose CT images are
typically acquired using a current of 30–50 mAs
and maximum tube voltage of 120–130 kVp [31].
Though attenuation map generation in hybrid
PET/CT scanners is straightforward, specic
strategies should be adopted to generate patientspecic attenuation maps on hybrid PET/MRI
scanners. Since the major challenge in MRIguided attenuation map generation is bone tissue
identication, zero-time echo (ZTE) MR
sequence was employed to acquire signals from
bony tissue to be included in the generation of
brain PET attenuation maps (this strategy is used
on the SIGNA™ PET/MRI scanner, GE
Healthcare) [
34]. Other approaches rely on a
temple of the human head to incorporate skull
bone in brain attenuation map initially estimated
from Dixon T1-weighted sequence (this strategy
is used on the Biograph mMR hybrid scanner,
Siemens Healthineers) [33].
Conventional ordered-subsets expectation
maximization (OSEM) algorithm is commonly
employed to reconstruct brain 68Ga-Pentixafor
PET images. Different iterations and subsets are
used across various centers, even on the same
PET scanners. For instance, 4/21, 3/21, and 3/24
iterations/subsets have been used to reconstruct
68
Ga-Pentixafor brain PET images on the
Biograph mCT and mMR scanners (Siemens
Healthineers) [14, 31, 33]. Image reconstruction
is carried out using time-of-ight (TOF) information and corrections for radioactivity decay, random coincidences, photon attenuation, and
Compton scatter. Resolution recovery or point
spread function (PSF) modeling is considered
within PET image reconstruction. The positron
range of 68Ga is about 3.5 mm FWHM, which
would lead to inferior spatial resolution in PET
imaging compared to short positron-range radiotracers, such as 18F-FDG (<1mm) [35]. The limited spatial resolution compared to the size of the
target structures in brain imaging would lead to
signicant partial volume effects. This would
adversely affect the quantication and quality of
PET images [
36]. The use of partial volume cor-
rection approaches, particularly anatomically
guided approaches involving the use of MR
images, would improve the quantication of
68
Ga-Pentixafor brain PET images. Post-
reconstruction smoothing is applied to
68
Ga-Pentixafor brain PET images to suppress
noise using a Gaussian lter with a kernel size
within the range 2–7.5 mm, depending on the
noise levels [14].
Whole-body 68Ga-Pentixafor PET scans are
normally conducted from the tip of the skull to
the middle thigh either in hybrid PET/CT or PET/
MR imaging. The administered radiopharmaceu-
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tical activity varies across different centers/protocols, wherein an activity within the range of
1.5–2.9MBq/kg is prescribed in 68Ga-Pentixafor
PET examinations [26]. Since 68Ga-Pentixafor
metabolism is not linked to the glycemic condition, no specic dietary preparation is required in
whole-body 68Ga-Pentixafor PET scans [37].
Most 68Ga-Pentixafor PET scans were conducted
60min post-injection ho. However, uptake times
between 30 and 120 min have been applied in
whole-body examinations [38, 39]. Depending
on the acquisition protocols, an acquisition time
of 2–5 min per bed position was adopted in
68
Ga-Pentixafor PET scans [38, 40]. For attenuation and scatter correction, PET acquisitions
were followed by unenhanced low-dose CT scans
on PET/CT scanners (20–50 mAs and 120–130
kVp) [29, 36]. On hybrid PET/MRI scanners,
synthetic CT images are generated from a twopoint MR Dixon (volume-interpolated
breath- hold T1-weight sequence) involving four
major tissue classes including background air,
lung, fat, and soft-tissue [41].
PET image reconstruction is carried out using
the conventional OSEM algorithm using mostly
3/21 iterations/subsets on the Biograph mMR
and mCT (Siemens Healthineers). The PET
emission data is corrected for randoms, decay,
photon attenuation, and scatter, and time-of-ight
information is considered within image reconstruction when available. Resolution recovery or
point spread function (PSF) modeling is applied
to enhance the spatial resolution of PET reconstructions. To reduce noise levels in
68
Ga-Pentixafor PET image reconstruction, a
post-reconstruction Gaussian lter with a kernel
of within 2–4mm is applied.
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