admp

[axelvento]

FDA Approves Trial of Adamis Pharmaceuticals Product Candidate to Treat Prostate Cancer - Yahoo! Finance

.24

[playars]

Alla fine hai tirato fuori la perla...

[axelvento]

si porta al mercato superiore....MAYBE


LONG$$$$$$$$$$$$$$$$$$$

[axelvento]

o/s81M
float47M

[axelvento]

studia per massacrare il cancro + indegno
Adamis Reports APC-300 Kills Human Pancreatic Cancer Cells

se trova la soluzione ADDIO$$$$$$$$$$$$$$$$$$

its drug APC-300 significantly inhibits the growth of pancreatic cancer cells. Pancreatic cancer still remains one of the most deadly forms of all cancers. The mortality from pancreatic cancer compares strikingly with its incidence. It has one of the worst prognoses with an overall survival rate of less than 5% and with most of the patients dying within the first two years. Recent results regarding the mechanism leading to the occurrence of pancreatic cancer suggest that in more than 90% of pancreatic cancers the Ras oncogene has been mutated. The mutation of the Ras oncoprotein has been linked to the induction of multiple signaling pathways within the cell which leads to the resistance of those cells to apoptosis (cell death) and the emergence of cancer.



In an attempt to understand how APC-300 works, Dr. Hasan Mukhtar and his team at the University of Wisconsin, have taken human pancreatic adenocarcinoma cells and investigated the effect of APC-300 on tumor cell growth and on the modulation of multiple Ras induced signaling pathways. APC-300 treatment of cancer cells was found to significantly reduce the expression of Ras oncoprotein and to modulate the protein expression of various signaling molecules involved in cancer cell growth. APC-300 attacks the cancer cells at multiple signaling pathways leading to tumor cell death and the inhibition of the growth of pancreatic cancer cells (Life Sciences, 2011 (88) pp. 285-293 and Cancer Res. 2009, 69(3) 1156-65.).



Additionally, in a mouse pancreatic cancer model, APC-300 was shown to significantly reduce the growth of tumors (p<0.01). Collectively, the data show that APC-300 induces apoptosis leading to the reduced tumorgenicity of human pancreatic cancer cells in the mouse tumor model and the killing of cancer cells in vitro. It is believed that one of the advantages of APC-300 is that it has the ability to intervene at more than one critical pathway in the pancreatic cancer cell process.



Dr. Dennis J. Carlo, Ph.D., President and CEO of Adamis states that, “Because of the known mechanisms of action of APC-300, and its ability to effect multiple signaling targets within the cancer cell, this drug will likely be active against different tumors. In fact, the data we have to date, support that to be the case.”

[axelvento]

Adamis Pharmaceuticals

LE PERLE esistono
BASTA SCOVARLE

[elisa999]

20K ci sono
0.24

[axelvento]

speriamo in bene ELISA....
a prestoooooooooooooooooooooo!

[playars]

news ieri
Adamis Vaccine Technology Granted a Patent in Europe - Yahoo! Finance

[axelvento]

Adamis Reports APC-300 Kills Human Prostate Cancer Cells


announced:
that in addition to activity in pancreatic cancer and its multiple modes of action, APC-300 significantly inhibits the growth of prostate cancer cells.



In 2010, the American Cancer Society reported that 217,730 men in the U.S. were diagnosed with prostate cancer and 32,050 were projected to die from the disease. While treatment with surgery and/or radiation is often successful, about one-third of patients will experience disease recurrence. Despite the initial success of androgen deprivation therapy (castration), prostate cancer continues to progress from androgen-dependent prostate cancer (ADPC) to castrate-resistant prostate cancer (CRPC) in most of these patients within a matter of years. More and more data point to the fact that androgen receptor (AR) plays a central role in both ADPC and CRPC. Therefore, identifying inhibitors of AR signaling which can act independent of hormonal status is of prime importance. These types of inhibitors could prove to be very important in the treatment of prostate cancer and thereby prevent or delay ADPC from progressing to CRPC. Based on the most recent information, APC-300 could very well be a molecule that acts independent of hormonal status.



A study published in Clinical Cancer Research (June 28, 2011) and authored by Dr. Mohammad Saleem and his associates from the Hormel Institute, University of Minnesota and the Mayo Clinic showed that APC-300 inhibits AR signaling and activation in prostate cancer in both ADPC and CRPC. Agents that have the potential to combat prostate cancer under both conditions (androgen and non-androgen responsive environments) are rare, but obviously desirable. APC-300 has been shown to have this desired activity. The results of the current study are significant because they demonstrate that APC-300, while sparing normal cells, preferentially inhibits the growth and proliferation of heterogeneous prostate cancer cells representing differential androgen sensitivity and AR expression status. Also, the observation that APC-300 sensitized highly aggressive CRPC cells to bicalutamide (currently used to treat ADPC) has high clinical relevance.



Additionally, APC-300 was shown to decrease messenger RNA and protein expression of the AR-target gene, PSA (biomarker for prostate cancer) in ADPC and CRPC cells. This translated into APC-300 showing a decrease in the secreted levels of PSA in a concentration dependent manner and a decrease in the growth of prostate cancer cells in vitro and in vivo. The data provide good evidence that APC-300 has the potential to decrease the AR transcriptional activity of ADPC and CRPC cells by blocking the AR occupancy on AR-responsive elements in target genes. The data also show that APC-300 had a significant effect on reducing the growth of ADPC and CRPC and reducing the levels of PSA in the mouse tumor model. Taken together, these data suggest that APC-300 may very well play a significant role in the treatment of prostate cancer.



Dennis J. Carlo, Ph.D., President and CEO of Adamis, states that, “We continue to build upon our prostate cancer franchise. New independent published data validate the importance of our three compounds (APC-100, 200, 300) for the treatment of prostate and pancreatic cancer. We will continue to focus and aggressively move these compounds into the clinic. Molecules such as APC-300 could very well work alone, but also just as important, APC-300 may enhance the activity of compounds already marketed and used for the treatment of prostate cancer.”