Immupharma PLC Update on Cancer Compound IPP-204106 'Nucant'
November 16 2016 - 2:01AM
RNS Non-Regulatory
TIDMIMM
Immupharma PLC
16 November 2016
RNS REACH : FOR IMMEDIATE RELEASE 16 NOVEMBER 2016
IMMUPHARMA PLC
Update on Cancer Compound IPP-204106 'Nucant'
Mechanism of Action Published in Prestigious Medical Journal
'Cancer Research'
ImmuPharma plc (LSE:IMM) ("ImmuPharma" or the "Company" or the
"Group"), the specialist discovery and development pharmaceutical
company, is pleased to announce that Cancer Research, the
prestigious medical journal of the American Association for Cancer
Research ("AACR"), has published a fundamental scientific paper
disclosing the mechanism of action of the Company's cancer compound
IPP-204106.
The IPP-204106 programme, which is a potential treatment for
various cancers, involves the development of synthetic peptides,
Nucants, which target surface nucleolin with very high affinity and
selectivity.
The publication was entitled "Nucleolin targeting impairs the
progression of pancreatic cancer and promotes the normalization of
tumour vasculature" and was authored by a number of researchers
working within ImmuPharma on the Company's Cancer programme.
The key findings of the study for this compound (referred to in
the paper as N6L) were:
-- Nucleolin inhibition is a new anti-cancer therapeutic
strategy that has been shown to dually normalise tumour vasculature
and reduce its volume
-- As a result, it has the potential to improve dramatically the
delivery and efficacy of existing chemotherapeutic drugs, and in
particular, for difficult-to-treat tumours such as Pancreatic
cancer
Dr. Robert Zimmer, MD, PhD, ImmuPharma's President and head of
R&D explains: "The publication of the mechanism of action of
the Nucants in Cancer Research is a validation of this novel
concept in the treatment of cancer we have been developing in
partnership with our collaboration partner, CNRS. It relies on the
modulating effect of the Nucants on angiogenesis, the mechanism
which controls the formation of micro vessels. Generally, the
tumour generated micro vessels are of poor quality and offer a poor
supply of blood and oxygen to the tumour. As a consequence, it
makes the tumour much more resistant to cytotoxic drugs. By
modulating the tumour micro vessels Nucants ameliorate the blood
flow, allow a better oxygen supply and increase the intra-tumoural
cytotoxic drug concentration. About threefold increase of cytotoxic
drug concentration and threefold decrease in tumour size have been
observed in preclinical studies. The intended treatment scheme is
to pre-treat the patient with Nucant and then deliver the standard
dose of cytotoxic drug, Gemcitabin for example in pancreatic
cancer.
This is the second time that we have been acknowledged by the
ACCR. The first in 2011 when our Cancer compound was chosen to be
on the cover of the journal disclosing the specific binding to
nucleolin and therefore to tumour cells by the Nucants. It is a
pleasing validation of years of research by our scientific team and
collaborators and gives us further confidence in the long term
potential of our Cancer programme, this compound and its unique
mechanism of action".
The publication can be seen at
http://cancerres.aacrjournals.org/content/early/2016/10/15/0008-5472.CAN-16-0300
and the website of Cancer Research is
http://cancerres.aacrjournals.org/
The 2011 publication can be seen at:
http://cancerres.aacrjournals.org/content/71/9/3296
The full 'Abstract' is detailed below:
"Pancreatic cancer is a highly aggressive tumour, mostly
resistant to the standard treatments. Nucleolin (NCL) is
overexpressed in cancers and its inhibition impairs tumour growth.
Herein we showed that NCL was overexpressed in human specimens of
pancreatic ductal adenocarcinoma (PDAC) and that the overall
survival significantly increased in patients with low levels of
NCL. The NCL antagonist N6L strongly impaired the growth of primary
tumours and liver metastasis in an orthotopic mouse model of PDAC
(mPDAC). Similar anti-tumour effect of N6L has been observed in a
highly angiogenic mouse model of pancreatic neuroendocrine tumour
RIP-Tag2. N6L significantly inhibited both human and mouse
pancreatic cell proliferation and invasion. Notably, the analysis
of tumour vasculature revealed a strong increase of pericyte
coverage and vessel perfusion both in mPDAC and RIP-Tag2 tumours,
in parallel to an inhibition of tumour hypoxia. NCL inhibition
directly affected endothelial cell (EC) activation and changed a
pro-angiogenic signature. Among the vascular activators, NCL
inhibition significantly decreased Ang-2 secretion and expression
in ECs, in the tumour and in the plasma of mPDAC mice. As a
consequence of the observed N6L-induced tumour vessel
normalization, pre-treatment with N6L efficiently improved
chemotherapeutic drug delivery and increased the anti-tumour
properties of gemcitabine in PDAC mice. In conclusion, NCL
inhibition is a new anti-pancreatic cancer therapeutic strategy
that dually blocks tumour progression and normalizes tumour
vasculature improving the delivery and efficacy of chemotherapeutic
drugs. Moreover, we unveiled Ang-2 as a potential target and
suitable response biomarker for N6L treatment in pancreatic
cancer".
-Ends-
For further information please
contact: + 44 (0) 20
ImmuPharma plc (www.immupharma.org) 7152 4080
Tim McCarthy, Chairman
Lisa Baderoon, Head of Investor
Relations + 44 (0) 7721
Twitter: @immupharma 413496
Panmure, Gordon & Co., (NOMAD +44 (0) 20
& Broker) 7886 2500
Freddy Crossley, Duncan Monteith,
Corporate Finance
Charles Leigh-Pemberton, Corporate
Broking
Northland Capital Partners Limited
(Joint Broker)
Patrick Claridge, David Hignell,
Corporate Finance
Rob Rees, John Howes, Corporate +44 (0)20 3861
Broking 6625
This information is provided by RNS
The company news service from the London Stock Exchange
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