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[schwi105]

Dyax Corp Home Page

Company: DYAX Corporation
Ticker: DYAX
Why Long: Strong results from Phase III clinical trials for DX-88 for Tx of HAE and recent FDA complete response letter (i.e. buy on the dip).
Buy-In: $2 or lower
Target SP: $3.50-$4 by December

This company recently received a Complete Response letter from the FDA:

Dyax Investor Relations

No further clinical trials were requested, just "a Risk Evaluation and Mitigation Strategy (REMS) and additional information with respect to the chemistry, manufacturing and controls (CMC) section of the BLA"

DYAX recently sent a response to the Complete Response Letter which the FDA accepted:

Dyax Investor Relations

Strong Phase III results:

Dyax Investor Relations

This stock has taken a recent beating due to the Complete Response Letter; however, no further clinical trials are needed (or so it appears), and the Phase III data look promising. The company appears to be working closely with the FDA to get this thing approved. I am getting in on this dip. I expect the SP to gradually rise from here. The CEO also recently purchased 10,000 shares (not huge, but a sign of confidence in this company's future):

Dyax Corp. (DYAX) CEO Gustav Christensen buys 10,000 Shares -- GuruFocus.com

The company appears to have made a turnaround from the recent dip, and I think this is a buy right now.

Some general company information from website:

Mission
Dyax’s mission is to discover, develop, and commercialize innovative biopharmaceuticals for unmet medical needs, while delivering outstanding value to patients and stockholders.

Strategy
Our therapeutic product candidates include fully human monoclonal antibodies as well as small proteins and peptides. Dyax is particularly focused on medical advances in the areas of oncology and inflammation. Our powerful discovery technology provides us the uncommon advantage of being able to both identify and then develop our own clinical leads. Our integrated approach also allows us to leverage this technology into revenue generating collaborations with other companies and researchers to further their own product pipelines.

History in Brief
The company was co-founded in 1995 by biotechnology entrepreneur Henry E. Blair, presently the Chairman, President and Chief Executive Officer of Dyax Corp. Dyax Corp. was formed by the merger between Biotage, a separations instrument chromatography firm, and Protein Engineering Corporation, from which we acquired our patented proprietary phage display technology. In 2003, Dyax sold its non-core business, Biotage, to focus exclusively on biotherapeutics.

Dyax Corp. issued an initial public offering (IPO) in August 2000 and is listed on the NASDAQ exchange (Ticker: DYAX). Our company is headquartered in Cambridge, Massachusetts.

Technology
Dyax’s core proprietary phage display technology allows for the rapid identification of compounds that bind with very high affinity and specificity to therapeutic targets. Utilizing phage display, we generate large diverse libraries of human antibodies, peptides, and proteins, which may be screened against disease-associated target molecules to identify potential binders. Automation allows us to rapidly screen these libraries for high-affinity binders. Our libraries’ vast size and diversity often yield multiple candidates, from which we can quickly select the single best therapeutic candidate.

HAE and DX-88 Information:

What is HAE?
Hereditary angioedema (HAE) is an acute inflammatory condition characterized by episodes of severe, often painful swelling affecting the extremities (hands, feet, face, etc.), the gastrointestinal tract, the genitalia, and in potentially life-threatening cases, the larynx. HAE is caused by low or dysfunctional levels of C1 esterase inhibitor (C1-INH), a naturally occurring molecule that inhibits kallikrein and other serine proteases in the blood.

Published estimates on the prevalence of HAE range from 1 in 10,000 to 1 in 50,000 adults and children around the world, with no known correlation to gender, ethnicity or geography.

HAE attacks vary in frequency and severity among patients, and each attack may manifest differently. The triggers of HAE attacks are not well understood, although factors such as physical trauma, stress, hormonal changes, oral surgery and cold weather are relatively well documented.

Untreated, HAE can be fatal; a laryngeal attack can rapidly close the airways, and facial attacks can progress to laryngeal. Abdominal attacks of HAE are extremely painful and often lead to nausea and vomiting caused by obstruction and swelling in the intestinal wall. Peripheral attacks are visually disfiguring. All types of HAE attacks are debilitating, affecting the activities of patients’ daily lives. On average, HAE patients have 12 attacks per year, which generally persist for 2 to 5 days before resolving on their own.

HAE is caused by an autosomal dominant mutation, which means that a parent with the disease has a 50% chance of passing it on to his or her offspring. Spontaneous mutations resulting in HAE occur, but more often, a patient with HAE represents one of several family members with the condition. Therefore, once a patient is properly diagnosed, a cluster of family members can also be identified.



Current Treatment of HAE
There is no marketed therapy for acute attacks of HAE in the United States. However, some adults with severe HAE manage the frequency of attacks with the chronic use of anabolic steroids. While this may reduce the number of attacks in some patients, steroids are ineffective during an attack and are associated with serious side-effects.

In some European countries, there is a marketed product for HAE. This product is human plasma-derived C1-INH, which replaces the missing or dysfunctional protein. However, it is isolated from human plasma and carries the potential risk of blood-borne pathogens. It is also a non-specific inhibitor of kallikrein, which is thought to be the most relevant target in HAE.



Why DX-88 in HAE?
Kallikrein is a key enzyme in the inflammatory cascade. It liberates bradykinin, a molecule that causes local leakage of fluid from the blood vessels into the tissues and is capable of producing the swelling and pain associated with HAE.

DX-88 is a small protein that powerfully and specifically inhibits kallikrein in laboratory experiments. Unlike C1-INH, it does not inhibit any other blood enzymes against which it was tested. Because it bypasses the C1-INH pathway, it shows potential in treating not just HAE but also other less common forms of non-allergic angioedema, and the acquired forms of angioedema (AAE) that can occur secondary to blood malignancies or autoimmune disease.



Clinical Trial Status of DX-88 in HAE

Trial Status
Dyax has completed three Phase 2 clinical trials, referred to as EDEMA0, EDEMA1®, and EDEMA2SM, and two Phase 3 trials, known as EDEMA3® and EDEMA4®, to evaluate DX-88 for its potential to treat HAE.

Completed Phase 2 Trials
EDEMA0, a 9-patient, multicenter, Phase 2, open-label dose-escalation study of DX-88 in HAE was initiated in 2001 at several European sites. Initial results from this study were announced in March 2003, demonstrating that all patients had clinical improvement of HAE attacks within four hours of treatment. The drug was generally well tolerated with the exception of an allergic reaction in one patient, whose HAE symptoms were resolved.

EDEMA1, a 48-patient, multicenter, Phase 2, placebo-controlled, single dose, dose-escalation study was completed in May 2004. Initial results from this lead trial were announced in June 2004 and demonstrated that DX-88 was significantly more efficacious than placebo in producing clinical improvement of HAE attacks within 4 hours of dosing (p=0.0169). Positive final results from EDEMA1 were announced in November 2004. The final results demonstrated that DX-88 was effective at treating HAE attacks at all anatomic locations, including life-threatening laryngeal attacks.

EDEMA2, a 77-patient, multicenter, Phase 2, open-label, repeat dosing trial was completed in January 2006. Two routes of administration, intravenous (IV) and subcutaneous (SC), were administered. The final results from the EDEMA2 trial were presented at the ACAAI Conference in November 2006 and reported on 240 HAE attacks in 77 patients using intravenous (IV) and subcutaneous (SC) routes of administration. Final results indicated that DX-88 provided substantial therapeutic benefit and can elicit rapid clinical response for HAE patients.

Completed Phase 3 Trials
EDEMA3, a 72-patient, multicenter, Phase 3, placebo-controlled trial was completed in November 2006. Topline results were announced in April 2007. The results showed that the primary and secondary endpoints demonstrated statistical significance. In addition, the overall safety results showed that DX-88 continues to be well tolerated. The trial was conducted to determine the efficacy of the 30 mg fixed subcutaneous (SC) dose of DX-88 for patients suffering from moderate to severe acute HAE attacks. The EDEMA3 trial was comprised of two phases: a double-blind, placebo-controlled phase and a repeat dosing phase. In the first phase, HAE patients received either a single 30 mg SC dose of DX-88 or placebo. After patients received one treatment in the placebo-controlled portion of the study, they were eligible for the second phase where they received repeat dosing with SC DX-88 for any subsequent acute attacks.

In June 2008, Dyax completed a second Phase 3 trial, EDEMA4, which was being conducted under a special protocol assessment (SPA). The trial design was based on EDEMA3 with an addition of a 4-hour rescue. The purpose of the trial was to further support the validity of the patient reported outcome (PRO) methodology and to confirm efficacy and safety.
Subcutaneous Formulation
The SC formulation was administered in the EDEMA2 and EDEMA3 trials and is also being administered in the EDEMA4 trial. This route of administration offers a relatively quick and simple method of dosing patients with DX-88, as compared to IV dosing. It is the Company’s expectation that a subcutaneously administered product can maximize the use and market potential of DX-88 for the treatment of HAE.

And the key piece of information is....drum role please.....

On 8/6/09, Dyax Corp. (NASDAQ:DYAX) announced today that the FDA accepted the Company's submission in response to the FDA's March 2009 Complete Response Letter (CRL), which outlined requirements for approval of DX-88 for the treatment of acute attacks of hereditary angioedema (HAE). In connection with the acceptance, the FDA assigned Dyax's BLA a new PDUFA action date of 12/1/09, which represents a six-month, Class 2 Review. In the CRL received 3/25/09, the FDA requested submission of a Risk Evaluation and Mitigation Strategy (REMS) and additional information with respect to the chemistry, manufacturing and controls (CMC) section of the BLA. Dyax believes these issues are fully addressed in its reply, which was submitted 6/1/09.

I like the potential.

Darin

[w00tw00t]

Interesting find but I think you could just sit down and wait for a moment before pouring you money into this one. The FDA date is in december and in 6months a lot can happen. I'm not very happy with the financials either but it could be me :p

[schwi105]

I agree, the financials are a little shaky and it may dip a bit lower; however, biotech stocks tend to have poor financials until they get a drug approved, and this thing was trading at double its lows in Jan./Feb. DYAX. I expect it to get back to the $3-$4 range prior to the new PDUFA date in December, so a solid 50% from current levels. It may dip a bit, but still a good guy at current prices.

Holding off for a bit might not hurt either. Thanks for the input.

Darin