Actually, there's one born every minute.eom

What is the Difference between EuroDNA™ 2.0 and other “Ethnogeographic” autosomal tests?

The difference is profound. The main difference is power – due to the large number of markers used and the work that went into selecting these markers from the human genome. Autosomal genetic tests are relatively new and a great advance over the Y chromosome and mtDNA test (which only report on a small fraction of your ancestors). However among the new autosomal tests, quality differs dramatically from EuroDNA™ 2.0. Discerning sub-European ancestry and admixture is very ambitious, and the research needed to find and develop the markers required was not inexpensive. Some groups have taken a “quick-and-dirty” approach and launched so-called "Ethnogeographical" DNA tests that use forensic markers called STRs for reporting sub-European ancestry from the autosomes. Usually, autosomal STRs are not selected from human DNA based on their ancestry information content, and so they provide less power. Because they lack this power, many of these tests are incapable of reporting admixture (such as 50% Iberian, 50% Basque), as opposed to primary affiliation (such as, “the sample belongs to group X”). Worse, the error associated with these other tests is not only dramatically higher, but primarily undocumented and undisclosed to customers. The power of using Ancestry Informative SNPs is that a very large collection can be screened, and large panels of highly informative markers can be assembled to provide the EuroDNA™ 2.0 test with unprecedented power. This power translates into accuracy and meaning, which other tests attempting to resolve European sub-ancestry lack. Further, we can precisely quantify the error so that customers know how to interpret their results. That the bases for most of these other tests for inferring ancestry have not been published – in papers detailing their performance, or as part of other papers where they have been used for this purpose - speaks volumes. The basis for the EuroDNA™ 2.0 panel of markers was published in the American Journal of Human Genetics earlier in 2007 (Bauchet et al., 2007) and, of course, the publication was peer reviewed.

http://ancestrybydna.com/welcome/productsandservices/eurodna/manual/index.php#e008

Statin-induced expression of CD59 on vascular endothelium in hypoxia: a potential mechanism for the anti-inflammatory actions of statins in rheumatoid arthritis.

Kinderlerer AR, Steinberg R, Johns M, Harten SK, Lidington EA, Haskard DO, Maxwell PH, Mason JC.

Cardiovascular Medicine Unit, Eric Bywaters Center for Vascular Inflammation, Imperial College London, Hammersmith Hospital, London, UK.

Hypoxia, which leads to dysfunctional cell metabolism, and complement activation both play central roles in the pathogenesis of rheumatoid arthritis (RA). Recent studies have reported that mice deficient for the complement-inhibitory protein CD59 show enhanced susceptibility to antigen-induced arthritis and reported that statins have anti-inflammatory effects in RA. We hypothesized that the anti-inflammatory effect of statins in RA relates in part to their ability to increase CD59 expression in hypoxic conditions and therefore to reduce complement activation. Flow-cytometric analysis showed that CD59 expression on endothelial cells (EC) was unaffected by atorvastatin in normoxia (21% O2), whereas in hypoxic conditions (1% O2) an up to threefold dose-dependent increase in CD59 expression was seen. This effect of hypoxia was confirmed by treatment of EC with chemical mimetics of hypoxia. The upregulation of CD59 protein expression in hypoxia was associated with an increase in steady-state mRNA. L-Mevalonate and geranylgeraniol reversed the response, confirming a role for inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase and geranylgeranylation. Likewise, inhibition by NG-monomethyl-L-arginine and NG-nitro-L-arginine methyl ester confirmed that CD59 upregulation in hypoxia was nitric oxide dependent. The expression of another complement-inhibitory protein, decay-accelerating factor (DAF), is known to be increased by atorvastatin in normoxia; this response was also significantly enhanced under hypoxic conditions. The upregulation of CD59 and DAF by atorvastatin in hypoxia prevented the deposition of C3, C9 and cell lysis that follows exposure of reoxygenated EC to serum. This cytoprotective effect was abrogated by inhibitory anti-CD59 and anti-DAF mAbs. The modulation of EC CD59 and DAF by statins under hypoxic conditions therefore inhibits both early and late complement activation and may contribute to the anti-inflammatory effects of statins in RA.

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=16859540&dopt=...

The most exciting area is our diabetes testing with Harvard Medical School. This is a product called glycated CD-59. We have three (3) ongoing clinical trials through Harvard Medical School in association with the Brigham, Massachusetts General Hospital, and the Joslin Diabetes Center. This is looking at this glycated CD-59 diagnostic test to see its prevalence in various tissues. We have found that prevalence, so we believe we have a diagnostic test that will be more effective and easier to use. We are looking at the urine analysis as well as the backup for that test. That is a USD$1 to $2 billion opportunity itself. We believe it is a powerful test, which would again be linked back to genetic ancestry. In other words, in the long-term, we are transforming into a pharmaceutical company. We have what we believe is a good portfolio of long-term growth and
short-term leash programs; at this point, the only thing we are lacking is capital.

http://www.wallstreetreporter.com/profile.php?id=24029

Cosmic, the identification of genes will complement DNAG's technology which is investigational at the haplotype level.

GNS & Moffit:

"The models will be simulated to identify key genes causally driving cancer progression and the relationships between those genes and endpoints such as recurrence and survival. "

This study is currently recruiting patients.
Verified by H. Lee Moffitt Cancer Center and Research Institute December 2006

Sponsors and Collaborators: H. Lee Moffitt Cancer Center and Research Institute
GlaxoSmithKline
Information provided by: H. Lee Moffitt Cancer Center and Research Institute
ClinicalTrials.gov Identifier: NCT00215956

Purpose
This is an open-label, single center, phase I study designed to determine the MTD or oral topotecan as a radiosensitizing agent in the treatment of rectal cancer patients. Sequential cohorts of three patients will be given increasing doses of oral topotecan and fixed doses of concurrent radiation (45GY) over five weeks. Condition Intervention Phase
Rectal Neoplasms
Drug: topotecan
Procedure: radiation
Procedure: surgery
Phase I

MedlinePlus related topics: Colorectal Cancer
Genetics Home Reference related topics: Colorectal Cancer
Study Type: Interventional
Study Design: Treatment, Non-Randomized, Open Label, Uncontrolled, Single Group Assignment, Safety/Efficacy Study
Official Title: A Phase I Study of Oral Topotecan as a Radiosensitizing Agent in Patients With Rectal Carcinoma
Further study details as provided by H. Lee Moffitt Cancer Center and Research Institute:Primary Outcome Measures:
Maximum Tolerated Dose of topotecan
side effect profile of topotecan

Secondary Outcome Measures:
response rate

Total Enrollment: 28 Study start: November 2001

This is an open-label, single center, phase I study designed to determine the MTD or oral topotecan as a radiosensitizing agent in the treatment of rectal cancer patients. Sequential cohorts of three patients will be given increasing doses of oral topotecan and fixed doses of concurrent radiation (45GY) over five weeks. The starting dose of oral topotecan is 0.25mg/m2 to be concomitantly administered with radiation (45Gy) x 5 days every week unless the radiation is interrupted for Holidays/Weekends or toxicity requiring treatment delays occurs.

A total of 25 doses is planned. Doses will be escalated in 0.15 mg/m2 increments thereafter in subsequent cohorts. Topotecan will be administered immediately before daily radiation.

All patients will undergo a rectal biopsy before treatment begins and during treatment. Tissue will be submitted to H. Lee Moffitt Cancer Center for tumor marker assays. Tissue from the excised tumor at the time of surgery will also be sent for the same studies. Between day 10 and 14 of treatment, colonoscopy/sigmoidoscopy is mandatory to ensure having a quantitative estimate of the tumor shrinkage and to obtain a repeat rectal biopsy. All patients will undergo radiation therapy concurrently with oral topotecan. Patients will receive 180 cGY per fraction to a total dose of 4500cGy(conventional fractionation) to the pelvis using a 3 or 4 filed technique and high energy photons. Standardized fields for rectal cancer will be used to include the true pelvis (mid sacrum to at least 2-3 centimeters below the inferior aspect of the tumor volume).

Patients will undergo surgery-either a low anterior resection, abdominoperineal resection or local excision. All patients will be offered postoperative adjuvant chemotherapy consisting of 5-Fluorouracil (F-FU) 350 mg/m2/day i.v. for 5 days administered every 28 days times four cycles. Immediately prior to the administration of 5-FU, leucovorin will be administered at a dose of 20 mg/m2/day i.v. push daily for 5 days every 28 days times four cycles.

http://clinicaltrials.gov/ct/show/NCT00215956;jsessionid=5EC34A5933569E65A2B8020A19C29E2A?order=9

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Melphalan/Topotecan
Through collaboration with the Moffitt Cancer Research Center in Tampa, FL, we are investigating the genetic basis of Melphalan/Topotecan (MT) response in multiple myeloma patients. MT is a chemotherapy that prevents the cell division that tumors need to grow but for some patients, normal doses do not elicit the desired effect. A genetic test for predicting MT response could help minimize the likelihood of multiple myeloma relapse.

--------------------------------------------------------------


ALKERAN (melphalan) also known as L-phenylalanine mustard, phenylalanine mustard, L-PAM or L-sarcolysin, is a phenylalanine derivative of nitrogen mustard. Melphalan is a bifunctional alkylating agent which is active against selective human neoplastic diseases.

GlaxoSmithKline Research Triangle Park, NC 27709

mean frog...spiteful frog...

you stated:

Similarly Frudakis wraps himself in the mantle of the science and pretends to speak for it. Those that can't understand the science but who are taken in by the man, believe he may lead, when in fact all he does is leverage the science for his own financial advantage.

Your unscrupulous, unrelenting, approach has led you to the blinders you now wear. Your personal attacks on Frudakis reveal your most noticeable weakness. If you would please comment on the technology...(which you deny); I'm sure it would add to the credibility you seek. lol

This study is currently recruiting patients.
Verified by H. Lee Moffitt Cancer Center and Research Institute April 2007

Sponsors and Collaborators: H. Lee Moffitt Cancer Center and Research Institute
Hoffmann-La Roche
Information provided by: H. Lee Moffitt Cancer Center and Research Institute
ClinicalTrials.gov Identifier: NCT00127036

Purpose
The purpose of this study is to determine if the investigators can predict the sensitivity or resistance of colon cancer to the two available first line chemotherapy agents. Treatment will consist of 2 drugs given intravenously every 3 weeks and 1 drug, in pill form, given for 14 days, with 1 week of rest. Patients will see the doctor for evaluation and treatment every 3 weeks until their disease progresses or they become disease-free. Condition Intervention Phase
Adenocarcinoma
Colon Cancer
Drug: Oxaliplatin 130mg/m2 intravenously (IV)
Drug: Bevacizumab 7.5 mg/kg IV
Drug: Capecitabine 825mg/m2 by mouth (po)
Drug: Irinotecan 240 mg/m2 IV
Phase II


Further study details as provided by H. Lee Moffitt Cancer Center and Research Institute:Primary Outcome Measures:
To develop a tumor tissue classifier that will predict response to XELOX + bevacizumab or XELIRI + bevacizumab

Secondary Outcome Measures:
To evaluate the overall survival of colorectal cancer (CRC) patients treated with XELOX + bevacizumab (Arm A) or XELIRI + bevacizumab (Arm B)
To assess the toxicity associated with Arms A and B

Total Enrollment: 150 Study start: October 2003

Colorectal cancer is the third largest cause of cancer mortality in the United States. The treatment of metastatic colorectal cancer is undergoing rapid improvement. Currently, there are two major chemotherapy regimens, which can both be combined with anti-angiogenesis treatment. These regimens are 5-FU + irinotecan and 5-FU + oxaliplatin. Each therapy has roughly similar rates of response, but it is unclear which specific therapy would benefit which patients. The advent of genome wide expression analysis provides a tool to analyze these differences. In the microarray analysis of colon cancer outcome trial, sponsored by the National Institutes of Health (NIH) and Moffitt Cancer Center, patients with newly diagnosed metastatic colon cancer are biopsied and samples are preserved in RNA later. Patients are then randomized to either one of two state of the art regimens: capecitabine + irinotecan + avastin (bevacizumab) or capecitabine + oxaliplatin + avastin. Response to chemotherapy, time to progression, and overall survival are end points of this trial. Once accrual of patients has been met, the investigators will compare genome wide expression patterns for each group.

http://clinicaltrials.gov/ct/gui/show/NCT00127036?order=1

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http://www.dnaprint.com/welcome/press/press_recent/2004/march_29/

stocky, some of these?

This study is currently recruiting patients.
Verified by National Cancer Institute (NCI) December 2006



Recruiting Carboplatin Plus Paclitaxel With or Without Continued Low-Dose Paclitaxel in Treating Patients With Early-Stage Ovarian Cancer
Condition: Ovarian Cancer
2. Recruiting Carboplatin and Paclitaxel With or Without Sorafenib in Treating Patients With Unresectable Stage III or Stage IV Melanoma
Condition: Melanoma (Skin)
3. Recruiting Sorafenib With or Without Paclitaxel and Carboplatin in Treating Patients With Recurrent Ovarian Cancer, Primary Peritoneal Cancer, or Fallopian Tube Cancer
Conditions: Fallopian Tube Cancer; Ovarian Cancer; Peritoneal Cavity Cancer
4. Recruiting Vaccine Therapy With Either Neoadjuvant or Adjuvant Chemotherapy and Adjuvant Radiation Therapy in Treating Women With p53-Overexpressing Stage II or Stage III Breast Cancer
Condition: Breast Cancer
5. Recruiting Combination Chemotherapy With or Without Radiation Therapy in Treating Patients With Recurrent Head and Neck Cancer That Cannot Be Removed By Surgery
Condition: Head and Neck Cancer


H. Lee Moffitt Cancer Center and Research Institute at University of South Florida, Tampa, Florida, 33612-9497, United States; Recruiting
Cancer Answers 800-456-7121 canceranswers@moffitt.usf.edu

type
moffitt paclitaxel

http://clinicaltrials.gov/ct/gui/action/ChangeQuery

Novartis, Celgene File Suit to Block Generic Ritalin
IP News Blog - 16 March 2007 - 12:35pm
Celgene, a Ritalin manufacturer, and Novartis, its distributor, have sued generic production company Abrika for patent infringement. Two separate complaints were filed in the U.S. District Court for the District of New Jersey and in the U.S. District Court for the District of Delaware. This action followed Abrika’s filing of a new drug application with a

http://ipnewsblog.com/index.php/2007/03/16/novartis-celgene-file-suit-to-block-generic-ritalin/

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DNAPrint Genomics Selects PT-502 Lead Research Compound for Development of Drug for Treating Depression
Market Wire, July, 2006
DNAPrint Genomics, Inc. (OTCBB: DNAG) today announced it has confirmed positive results in an animal model for anti-depressant activity for its PT-502 lead compound being developed with the Massachusetts College of Pharmacy and Health Sciences.

"The results of the assay are encouraging and have enabled us to select PT-502 as the lead candidate for a new anti-depressant therapy," stated Dr. Mark Froimowitz, Research Professor of Chemistry at the Boston College. "The test results clearly show that PT-502 is active in a widely used animal assay for anti-depressant activity. This approach uses the dopamine system as a means of treating depression and is different from traditional serotonin and norepinephrine reuptake inhibitors such as Prozac(TM)."

In October 2005, DNAPrint Genomics announced that it has licensed a series of Ritalin(TM)-like compounds developed by Dr. Froimowitz. Ritalin(TM) is a well-known drug used for the treatment of attention deficit hyperactivity disorder (ADHD). These compounds have the potential to be enhanced pharmaceuticals for the clinical treatment of depression, drug addiction and ADHD.

Dr. Froimowitz noted that anywhere from 30% or more of the patients treated with available anti-depressants either do not respond to treatment or have adverse side effects. "PT-502 is our new compound designed to selectively block the reuptake of dopamine with a slow onset, and a longer duration of action. This pharmacokinetic profile indicates that PT-502 should have little or no abuse potential. This offers a new model for the treatment of depression that affects nearly 20 million people a year in the U.S. alone. Finding a treatment that may augment or enhance the use of serotonin and norepinephrine reuptake inhibitors could help millions of people suffering with depression."

Jever, yes the competition. I'll spin this as: The competition also validates the future and pressure on Big Pharma.

Celera and Collaborators Discover a Genetic Marker Associated with Severe Coronary Artery Disease
Thursday June 14, 4:05 pm ET
Carriers of Gene Variant Exhibit an Approximate 3-Fold Increased Risk of Disease
Findings from Three Studies Involving More Than 3,000 Individuals Likely to Improve Identification of High Risk Individuals Enabling Earlier Therapeutic Intervention


"The determinants of the severity of coronary artery disease are complex, but scientifically rigorous studies such as this one provide sound evidence of a major genetic component," said Stephen G. Ellis, M.D. Director, Sones Cardiac Department of Cardiovascular Medicine, and Professor of Medicine at the Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, a collaborator and a co-author of the study. "Eventually, building on these studies, physicians and patients should have access to blood tests that can assess each individual's respective genetic risk of developing this disease, which in turn will enable earlier therapeutic intervention."

"Large scale studies like this one, with well-characterized samples from carefully selected patients, allow the identification of genetic markers for risk of early-onset coronary artery disease, which could potentially be incorporated into individual risk assessment protocols," said Tom White, Ph.D., Chief Scientific Officer at Celera. "It may be possible for people at risk to ameliorate this genetic risk by undertaking well-established preventive measures. Celera is currently in licensing discussions with several laboratories about offering a test based on these discoveries."


http://biz.yahoo.com/bw/070614/20070614005829.html?.v=1

In my opinion... If Big pharma is staving off the future of medicine, that would certainly raise ethical questions. DNAG technology is in its' infancy...once validated by the likes of Harvard, St. Judes, Emory, Moffitt, M.D. Anderson, Neocodex, the FDA will have to push the buttons on Big Pharma.

I agree...eom

Give the people on this board a little credit. Some have been around a long time. Most are way down. And frankly, being invested in this stock has more to due with intuition than it does with country clubs and tea. Time for a beer...

mbmun, with proper financing, and partnerships in place...a $100-150 million market cap would be reasonable. JMHO

What exactly are you asking for? And then, get a grip. You're sounding irrational... like the guy in the movies that gets his face slapped.

JUNE 27, 2007

Moffitt looking for participants in new ovarian cancer trial

Tampa, Florida - Women suffering from recurrent ovarian cancer may have a new treatment regimen that may increase the response to treatment and prolong their lives. Doctors at H. Lee Moffitt Cancer Center & Research Institute are testing a combination of chemotherapy and the drug Avastin in these patients. Moffitt opened a clinical trial recently and is looking for new participants for the study.

Dr. Robert Wenham/Gynecologic Oncology Program at Moffitt
“We can often get the cancer to shrink for periods of time, but ultimately, it becomes resistant to standard chemotherapies. The hope is that by using these targeted therapies, we can prolong and manage the cancer making it more of a chronic disease process rather than something that's going to take the patient's life.”
The clinical trial will address ovarian cancers that are incurable and tough to treat. It will target women whose cancer has returned in the first year after initial treatment. Some data shows the new targeted therapy leads to higher responses and better survival than traditional chemotherapy drugs alone.

Dr. Robert Wenham/Gynecologic Oncology Program at Moffitt
“Avastin targets the molecules that cancers use to grow new blood vessels. Therefore, it chokes the cancer off.”
Moffitt is looking for clinical trial participants who have a recurrence or progression of ovarian cancer within a year of prior platinum chemotherapy. These women may have had up to two prior chemotherapy regimens for this malignancy. For more information on participating in the clinical trial, call (813) 745-7272.

H. Lee Moffitt Cancer Center & Research Institute & Tampa Bay's 10 News

http://www.tampabays10.com/news/local/article.aspx?storyid=57703

johnnyfiber: 1.4 million. eom

I interpreted this incorrectly. Thanks again.

Once they can get an IRB and the FDA to Ok a trial and an NDA, they can move forward and attempt to collaborate and partner on the myriad of technolgies in the pipeline IMHO.

Were there any questions asked along the lines of the technology being too broad at this point? A patients predisposition to disease...unable to be determined definitively at this level of technology? TIA

Are you saying there was blame being placed on the FDA for holding up research?

Precious, were there any updates on the research being conducted? Ovanome at Neocodex, Statnome, PONV, cd-59, the work being conducted at Moffitt, Emory...etc... Are cytokines going to be the next step incorporated into the company's methods? thanks

Precious,

There are over 550 million shares outstanding, and a huge number were taken off the potential market by them retiring them if what I heard was correct about that.
Karen Surplus stated that there were 12,00 shareholders up from 4-5,000 a few years back and I actually saw the list of Institutional holders only because where I sat, the alcove table had them on there under proxy info header and believe me there are some highly, highly prestigious firms that own huge amounts of DNAG shares, yet they won't fund it?????

The last 10k, I believe, stated there were 1,034 holders of common.

Retiring shares? Can you elaborate? TIA

Raymond James Downgrades Merck (MRK) to Market Perform
06-20-2007 09:35:17 AM
Raymond James downgrades Merck (NYSE: MRK) from Strong Buy to Market Perform.

Stocks Mentioned
MRK: $48.34
Change ($): -0.21
Change (%): -0.43
Volume: 11232640

Michael Krensavage, an analyst with Raymond James & Associates who covers the drug industry, said Merck's affiliation with Moffitt makes sense.

"All drug companies are looking for new medicines. They've had difficult times replacing the ones that have gone by the wayside," he said. "And Merck, in my opinion, is making a more concerted effort in cancer."

http://www.sptimes.com/2006/12/19/Tampabay/Moffitt__Merck_join_f.shtml

...the three headed toad...donning the mark of satan upon each split wart...

and then it reared its' ugly head...and it spoke in obfuscated phrases with a predisposition to invagle and deceive.

Precious, was ther any discussion along the lines of the company protecting itself from a takeover. It wouldn't take much to acquire a large chunk in the open market. Why hasn't big Pharma gone that route?

YES! Thank you, PreciousLife1. Much appreciated. It all sounded a lot better than I was expecting. It's renewed my faith in the Company.

nonsense...

So what...details elude you...

http://www.usic.net/UserFiles/File/USIC_E-NOTES_May_4_-_2007.pdf

DNAPrint Genomics, of Sarasota, Florida, is an applied
science company focused on development and marketing of
innovative genetic testing products and services. The
company’s research is aimed at discovery of DNA analysis
solutions to serve clients in forensic science, genealogical
research, and pharmaceutical development. As part of the
GSEC Law Enforcement Initiative, DNAPrint Genomics is
working with Lawrence Berkeley National Laboratory and
Engelhardt Institute of Molecular Biology (Moscow) to
develop a biological microchip technology for individual
genetic characterization in forensic genetic testing and
building of DNA databases.

poor mouther...tis not a pipe...rule 144 applies and is stated clearly in the "registration statement" Please stop belching your half-witted nonsense.



there are no agreements or arrangements under which the Company or any of its Subsidiaries is obligated to register the sale of any of their securities under the 1933 Act (except the Registration Rights Agreement);


REPORTS UNDER THE 1934 ACT.




With a view to making available to the Investor the benefits of Rule 144 promulgated under the 1933 Act or any other similar rule or regulation of the SEC that may at any time permit the Investor to sell securities of the Company to the public without registration (“Rule 144”), provided that the Investor holds any Registrable Securities are eligible for resale under Rule 144 (k), the Company agrees to:





8





--------------------------------------------------------------------------------




(a)

make and keep public information available, as those terms are understood and defined in Rule 144;




(b)

file with the SEC in a timely manner all reports and other documents required of the Company under the 1933 Act and the 1934 Act so long as the Company remains subject to such requirements (it being understood that nothing herein shall limit the Company’s obligations under Section 5(c) of the Investment Agreement) and the filing of such reports and other documents is required for the applicable provisions of Rule 144; and




(c)

furnish to the Investor, promptly upon request, (i) a written statement by the Company that it has complied with the reporting requirements of Rule 144, the 1933 Act and the 1934 Act, (ii) a copy of the most recent annual or quarterly report of the Company and such other reports and documents so filed by the Company, and (iii) such other information as may be reasonably requested to permit the Investor to sell such securities pursuant to Rule 144 without registration.




Section 9. NO ASSIGNMENT OF REGISTRATION RIGHTS.




The rights and obligations under this Agreement shall not be assignable.




Section 10. AMENDMENT OF REGISTRATION RIGHTS.




The provisions of this Agreement may be amended only with the written consent of the Company and Investor.




Section 11. MISCELLANEOUS.




(a) Any notices or other communications required or permitted to be given under the terms of this Agreement that must be in writing will be deemed to have been delivered (i) upon receipt, when delivered personally; (ii) upon receipt, when sent by facsimile (provided a confirmation of transmission is mechanically or electronically generated and kept on file by the sending party); or (iii) one (1) day after deposit with a nationally recognized overnight delivery service, in each case properly addressed to the party to receive the same. The addresses and facsimile numbers for such communications shall be:




If to the Company:




DNAPrint Genomics, Inc.

1621 West University Parkway

Sarasota, FL 34243

Telephone: (941) 366-3400

Facsimile: (941) 952-9770




If to the Investor:




Dutchess Private Equities Fund, Ltd.

50 Commonwealth Ave, Suite 2

Boston, MA 02116

Telephone: (617) 301-4700

Facsimile: (617) 249-0947




Each party shall provide five (5) business days prior notice to the other party of any change in address, phone number or facsimile number.




(b) Failure of any party to exercise any right or remedy under this Agreement or otherwise, or delay by a party in exercising such right or remedy, shall not operate as a waiver thereof.


http://us1.institutionalriskanalytics.com/SEC/SEC_DOC.asp?b=&doc=edgar/data/1127354/0001354488-0...

Under the new agreement the stock is not put to Dutchess. It was purchased as debt and is restricted. What part don't you understand?

like I said...buffoon. eom

3c, it's not the MM's...and it's not these idiots bashing.eom

cottonbuffoon... could you please enlighten me, in detail, regarding the latest "Investment Agreement" b/w Dutchess and DnaPrint. TIA

INVESTMENT AGREEMENT

INVESTMENT AGREEMENT (this "AGREEMENT"), dated as of March 30, 2007 by and between DNAPrint Genomics, Inc. a Utah corporation (the "Company"), and Dutchess Private Equities Fund, Ltd., a Cayman Islands exempted company (the "Investor").

WHEREAS, the parties desire that, upon the terms and subject to the conditions contained herein, the Investor shall invest up to Ten Million dollars ($10,000,000) to purchase the Company's Common Stock, $0.01 par value per share (the "Common Stock");


In the absence of the registration statement to which this prospectus is a part, certain of the selling stockholders would be able to sell its shares only pursuant to the limitations of Rule 144 promulgated under the Securities Act.


http://us1.institutionalriskanalytics.com/SEC/SEC_DOC.asp?b=&doc=edgar/data/1127354/0001354488-0...

That insiders have been accumulating, suggests to me: the upcoming restructuring will increase the share price from current levels.