Nein, die Finanzierungszusicherung kommt nicht von BICYPAPA sondern von Hopp
Der Kurs drohte ja schon einzuschlafen ...
|
Nein, die Finanzierungszusicherung kommt nicht von BICYPAPA sondern von Hopp
Der Kurs drohte ja schon einzuschlafen ...
Hallo BICYPAPA,
ich verstehe nicht recht wie du das mit den 35 Mio Aktien meinst? Kapitalerhöhung?
"Ich lege die Aktienanzahl zum März 2022 mit etwa 35 Millionen Stücken fest..."
"Doch mit meiner Prognose zur Aktienanzahl in meiner letzten Analyse hatte ich schon mal Recht. Das ist auch schon mal was. "
Schönes WE! Gruß Matze 91
...AACR Anual Meeting präsentiert wurden stehen auf der Hompage von HDP bereit.
Wissenschaftliche Poster (heidelberg-pharma.com)
Hier jeweils das Fazit:
Amanitin-based ADCs targeting PSMA as novel therapeutic modality for prostate cancer therapy:
Prostate cancer is one of the most common types of cancer in men world wide. PSMA is a type II membrane glycoprotein which is expressed on secretory cells within the prostatic epithelium and in nearly all prostate cancers (4). Elevated expression of PSMA correlates with tumor aggressiveness and tumor stage rendering PSMA an ideal target for prostate cancer treatment. In the current study, in vitro and in vivo data of amanitin based ADCs (ATACs) targeting PSMA with both a cleavable linker and a non-cleavable linker are presented. The promising potential of ATACs targeting PSMA is reflected by the high cytotoxic potency of anti-PSMA THIOMABS® on different PSMA + cell lines. Data presented underscores an effective and persistent anti-tumor activity of anti-PSMA ATACs in mouse xenograft models: Single dose treatment with ATACs employing different linker designs caused dose dependent tumor regression including complete tumor remission. Safety profiling in cynomolgus monkeys revealed good tolerability and therapeutic index for anti-PSMA ATACs. The use of amatoxins and the inhibition of RNA polymerase II as novel mode of action for ADCs not only results in apoptosis of dividing cells, but also of slowly growing and dormant cells. Based on its activity on drug resistant cells independent of the expression of multi-drug resistance transporters amatoxins possess the ability to overcome resistance as prerequisite for a long-lasting antitumor efficacy even in slow proliferating prostate cancers.
The positive findings of these experiments warrant the clinical development of anti-PSMA ATACs.
Combination of Antibody-Targeted Amanitin Conjugates (ATAC) with Immune checkpoint inhibitors shows a synergistic therapeutic effect in vivo:
ATAC treatment results in a complete and persistent anti-tumor effect in
vivo in different cancer entities, including heterogeneous PDX models that
cannot solely be explained by the toxicity of a-Amanitin. Especially, as a
direct bystander effect can be excluded due to the hydrophilic nature of
amanitin. Thus, the possibility of immune activation by ATAC treatment
was investigated in this study.
ATAC treatment resulted in ICD in vitro in multiple tumor models (data
shown for breast cancer). Furthermore, if mice that achieved complete
and stable tumor remission by ATAC treatment were re-challenged with
the same tumor cells, the tumor take rate was significantly reduced
compared to the first inoculation. These findings may suggest a possible
immune activation by ATAC treatment.
As all mouse strains used in in vivo studies were immune deficient but
maintained functional NK cells and as it is well known that NK cells can
induce tumor cell killing, a possible involvement of NK cells in the antitumor effect of ATACs was investigated. NK cell killing assays
demonstrated that ATAC treatment can potentiate NK cell activation. 50%
depletion of NK cells in vivo resulted in increased tumor re-take after ATAC
treatment in different cancer models while NK cell depletion did not affect
tumor growth in untreated mice. This data suggest that NK cells can
potentiate the anti-tumor effect of ATACs.
To investigate if this immune activation can be used for therapeutic
purposes, ATAC treatment was combined with immune checkpoint
inhibition in a humanized mouse model. Combined treatment with ATACs
and ICIs resulted in a synergistic anti-tumor effect in a s.c. Burkitt
lymphoma model that was co-injected with human PBMCs. This effect was
dependent on the presence of human immune cells as combined
treatment did not have a beneficial effect in the absence of human
PBMCs.
Taken together, the data presented provide a rationale to the use of ATACs
in combination therapy with immune checkpoint inhibitors.
Preclinical evaluation of anti-CD37 Antibody Targeted Amanitin Conjugates (ATAC) in B-cell malignancies:
Lymphoma is the most common lymphoid malignancy (4). It is a
heterogenous entity including B-cells which overexpress CD37. This
transmembrane protein of the tetraspanin superfamily is involved in different
biological processes (5). Because of its abundant overexpression on different
blood malignancies which include B-cells, CD37 is an ideal target to treat Bcell lymphoma.
In the current study, in vitro and in vivo data of an amanitin based ADC (ATAC)
with cleavable and stable linker targeting CD37 are presented. On different
CD37 + cell lines, both anti-CD37 ATACS showed strong cytotoxic potential with
EC50 values in the nanomolar range.
In two independent mouse xenograft models the used anti-CD37 ATACs
showed strong and persistent anti-tumor activity. Even the treatment with
low doses of both ATACs (MTD 1/16 of non-cleavable linker; MTD 1/10 of
cleavable linker) resulted in an 80% and 70% survival rate, respectively.
Given the results of the safety profiling in cynomolgus monkeys which have
proven a good tolerability and therapeutic index for both anti-CD37 ATACs,
amanitin as a toxic warhead for ADCs targeting CD37 on B cells could
represent a viable therapeutic option to treat B-cell malignancies. Through its
unique mode of action, ATACs are not only suited to target dividing cells, but
also slowly growing cells and dormant cells. Amanitin is also effective in drug
resistant cells, independent of the expression of multi-drug resistance
transporters. This is a potential advantage for amatoxin payloads in slow
proliferating B-cell malignancies, including mantel cell lymphoma.
The findings of these experiments warrant further clinical development of
anti-CD37 ATACs.
VG
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8 | 2.737 | Heidelberg Pharma AG | BICYPAPA | Guru51 | 24.04.24 17:29 | |
4 | 122 | Heidelberg Pharma | BICYPAPA | BICYPAPA | 13.12.23 17:23 | |
15 | 1.369 | Wilex könnte die 10euro erreichen!! | Nero. | Nero. | 25.04.21 13:30 | |
2 | Der Aktionär 48/18; Artikel zu Heidelberg Pharma | moggemeis | 24.04.21 23:02 | |||
10 | Heidelberg Pharma | Maydorn | tulmin | 19.03.20 09:10 |