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SEC Company Response from KERYX BIOPHARMACEUTICALS INC (CIK 0001114220) — Aug 12, 2005

KERYX BIOPHARMACEUTICALS INC (CIK 0001114220)
Date: Aug. 12, 2005 · CIK: 0001114220 · Accession: 0000950123-05-009893

AI Filing Summary & Sentiment

File numbers found in text: 000-30929

Referenced dates: July 29, 2005

Date
August 12, 2005
Author
Not clearly detected
Form
CORRESP
Company
KERYX BIOPHARMACEUTICALS INC (CIK 0001114220)

Letter

August 12, 2005 VIA: UPS AND EDGAR Mr. Jim B. Rosenberg Senior Assistant Chief Accountant United States Securities and Exchange Commission 100 F Street, N.E. Division of Corporation Finance Mail Stop 6010 Washington, D.C. 20549

Re: Keryx Biopharmaceuticals, Inc. Annual Report on Form 10-K for the year ended December 31, 2004 File No. 000-30929

Dear Mr. Rosenberg:

At the request and on behalf of our client, Keryx Biopharmaceuticals, Inc. (the "Company"), we hereby file, via EDGAR, responses to the Commission's comment letter dated July 29, 2005, relating to the Company's Annual Report on Form 10-K for the year ended December 31, 2004 (File No. 000-30929). These responses have been prepared by the Company with the assistance of its legal counsel. As requested, these responses are keyed to correspond to the Commission's comment letter. A copy of this letter is being sent to the Commission via overnight mail.

Comment:

Item 7. Management's Discussion and Analysis of Financial Condition and Results of Operations

Please refer to the Division of Corporation Finance "Current Issues and Rulemaking Projects Quarterly Update" under section VII - Industry Specific Issues - Accounting and Disclosure by Companies Engaged in Research and Development Activities. You can find it at the following website address: http://www.sec.gov/divisions/corpfin/cfcrq032001.htm. <TABLE> <S> <C> <C> <C> One Atlantic Center Bank of America Plaza 3201 Beechleaf Court, Suite 600 601 Pennsylvania Avenue, N.W. 1201 West Peachtree Street 101 South Tryon Street, Suite 4000 Raleigh, NC 27604-1062 North Building, 10th Floor Atlanta, GA 30309-3424 Charlotte, NC 28280-4000 919-862-2200 Washington, DC 20004-2601 404-881-7000 704-444-1000 Fax: 919-862-2260 202-756-3300 Fax: 404-881-7777 Fax: 704-444-1111 Fax: 202-756-3333 </TABLE> <PAGE>

Page 2

Please disclose the following information for each of your major research and development projects:

(a) The costs, including amounts recognized as acquired in-process research and development, incurred during each period presented and to date on the project;

(b) The nature, timing and estimated costs of the efforts necessary to complete the project;

(c) The anticipated completion dates; and finally

(d) The period in which material net cash inflows from significant projects are expected to commence.

Regarding (a), please disclose the significant assumptions used in valuing the acquired in-process research and development. If you do not maintain any research and development costs by project, disclose that fact, explain why management does not maintain and evaluate research and development costs by project, and provide other quantitative or qualitative disclosure that indicates the amount of the company's resources being used on the project.

Regarding (b) and (c), disclose the amount or range of estimated costs and timing to complete the phase in process and each future phase. To the extent that information is not estimable, disclose those facts and circumstances indicating the uncertainties that preclude you from making a reasonable estimate.

Response:

The Company proposes to include disclosure in the following general format in its Annual Report on Form 10-K for the year ending December 31, 2005, completed and updated accordingly at that time.

Response to comment (a)

Research and development costs for the years ended December 31, 2004, 2003 and 2002 were $[_________], $[_________] and $[_________], respectively. Research and development expenses consist primarily of salaries and related personnel costs, fees paid to consultants and outside service providers for clinical and laboratory development, facilities-related and other expenses relating to the design, development, testing, and enhancement of our product candidates and technologies, as well as expenses related to in-licensing of new product candidates. We expense our research and development costs as they are incurred.

The following table sets forth the research and development costs per project for the periods presented. <PAGE>

Page 3

Years ended December 31, ------------------------------------------------------- Cumulative, as of of December 2004 2003 2002 31, 2004 ---------- ---------- ---------- -----------------

KRX-101................. [______] [______] [______] [______]

KRX-0401................ [______] [______] [______] [______]

Other Drug Candidates... [______] [______] [______] [______] -------------------------------------------------------------------------------- Total Research and Development Costs....... [______] [______] [______] [______]

As required by FASB Interpretation No. 4, "Applicability of FASB Statement No. 2 to Business Combinations Accounted for by the Purchase Method" ("FIN 4"), the Company recorded a non-recurring, non-cash charge in 2004 of $18,800,000 for the portion of the purchase price of ACCESS Oncology, Inc. allocated to acquired in-process research and development. Of the $18,800,000 charge, [__________] relates to the portion of the purchase price allocated to KRX-0401, and the remaining [__________] relates to the portion of the purchase price allocated to the Company's other drug candidates acquired from ACCESS Oncology, Inc.

A project-by-project valuation using the guidance in SFAS No. 141, "Business Combinations" and the AICPA Practice Aid "Assets Acquired in a Business Combination to Be Used In Research and Development Activities: A Focus on Software, Electronic Devices and Pharmaceutical Industries" was performed with the assistance of independent valuation specialists to determine the fair value of research and development projects of ACCESS Oncology which were in-process, but not yet completed.

The fair value was determined using the income approach on a project-by-project basis. This method starts with a forecast of the expected future net cash flows. These cash flows are then adjusted to present value by applying an appropriate discount rate that reflects the project's stage of completion and other risk factors. These other risk factors can include the nature of the product, the scientific data associated with the technology, the current patent situation and market competition.

The forecast of future cash flows required the following assumptions to be made:

o revenue that is likely to result from specific in-process research and development projects, including estimated patient populations, estimated selling prices, estimated market penetration and estimated market share and year-over-year growth rates over the product life cycles;

o cost of sales related to the potential products using industry data or other sources of market data; <PAGE>

Page 4

o sales and marketing expense using industry data or other sources of market data;

o general and administrative expenses; and

o research and development expenses.

The valuations are based on information that is available as of the acquisition date and the expectations and assumptions that have been deemed reasonable by our management. No assurance can be given, however, that the underlying assumptions or events associated with such assets will occur as projected. For these reasons, among others, the actual results may vary from the projected results.

The Company will include the information in this response to comment (a) in its next Annual Report on Form 10-K for the year ending December 31, 2005, in Item 7, under a section entitled "Research and Development."

Response to comments (b) and (c)

The Company included the information below in its Annual Report on Form 10-K for the year ended December 31, 2004, in Item 1, under a section entitled "Products Under Development," except for the text underlined and included below. The Company will update the information accordingly for inclusion in its Annual Report on Form 10-K for the year ending December 31, 2005.

KRX-101

Overview

We have obtained a license to develop sulodexide, or KRX-101, to treat diabetic nephropathy and other conditions. Diabetic nephropathy is a long-term complication of diabetes in which the kidneys are progressively damaged. Sulodexide, our lead drug candidate, is a glycosaminoglycan compound with structural similarities to the broad family of marketed heparins and low molecular weight heparins. Specifically, sulodexide is comprised of heparan sulfate, also referred to as fast-moving heparin, dermatan sulfate and slow-moving heparin. This drug has been marketed in a number of European, Asian and South American countries for many years by our licensor for certain cardiovascular conditions and has a well established safety profile at the doses used for such indications. Additionally, it has been demonstrated in multiple clinical trials conducted in Europe, including a randomized, double-blind, placebo-controlled Phase II study, that KRX-101 can reduce urinary protein excretion in patients with diabetic nephropathy. In the fourth quarter of 2003, we announced the initiation of our KRX-101 U.S.-based Phase II/III clinical program for the treatment of diabetic nephropathy. In the third quarter of 2004, we completed the target enrollment for the Phase II portion of this clinical program. This trial is being conducted by the CSG. In January 2005, we announced that the CSG, based <PAGE>

Page 5

on a safety and efficacy analysis of the interim Phase II data conducted by an independent DSMC and the CSG, respectively, recommended that we proceed to the Phase III portion of our Phase II/III clinical program of KRX-101 for the treatment of diabetic nephropathy, as planned.

We plan to develop sulodexide in the United States, and possibly other countries where we have exclusive rights under our license, for the treatment of diabetic nephropathy and potentially for other indications.

Market Opportunity

According to the American Diabetes Association, or ADA, there are 18.2 million people in the United States, or approximately 6.3% of the population, who have diabetes. Of this population, approximately 13 million have been diagnosed with the disease, of whom approximately 90-95% have been diagnosed with diabetes mellitus, type 2, referred to as DM2. DM2 results from the combination of insulin deficiency and the body's relative insensitivity to the insulin present, as opposed to DM1, in which severe insulin deficiency results from destruction of the insulin-producing beta cells of the pancreas. Moreover, an August 2003 study published by Datamonitor estimates that approximately 50% of all diabetics in the U.S., or approximately 9 million people, have diabetic nephropathy. Diabetes is the most common cause of End Stage Renal Disease, or ESRD, in the United States and in many other developed nations and represents approximately 45% of all new cases of ESRD in the United States. Despite advances in clinical care, including improvements in glycemic or blood sugar control and blood pressure control, the number of DM1- and DM2-related cases of ESRD continues to rise. In particular, the incidence of DM2-related ESRD is rapidly increasing. Less than 20% of diabetics on dialysis in the United States survive for five years, making the mortality of end-stage renal failure in this group higher than most forms of cancer. Unfortunately, renal transplantation is an option for less than 20% of diabetics with ESRD, as compared to 40-50% of non-diabetics, principally due to age and concomitant vascular disease. Despite recent advances, diabetic nephropathy remains a potentially catastrophic illness, for which partial but insufficient treatment is currently available.

Scientific Background

Both DM1 and DM2 are characterized by insufficient insulin effect upon insulin-requiring tissues. As insulin is required for normal metabolism of glucose, fat and protein, diabetes is accompanied by abnormal blood levels of these substances. In the short term, hyperglycemia, or elevated blood glucose, causes the classic symptoms of diabetes: excessive thirst, frequent urination and weight loss. In the long term, hyperglycemia, as well as other effects resulting from insufficient insulin effect, can progressively damage critical anatomic structures resulting in chronic diabetic complications. We are developing sulodexide for the treatment of diabetic nephropathy, a long-term complication of diabetes in which the kidneys are progressively damaged. This progressive damage results in diminished kidney function progressing to ESRD, which ultimately leads to death unless treated by dialysis and/or renal transplant. <PAGE>

Page 6

The kidney consists of two anatomically and functionally distinct components placed in serial configuration. The first component is the glomerulus, which performs the critical filtering function of the kidney. Blood is passed through delicate microscopic glomerular capillary loops, which, acting as sieves, allow waste chemicals and excess water to pass through into the glomerular filtrate while retaining desirable components, such as blood cells and albumin, within the blood. One of the key components of the glomerular capillary filtering membrane is highly anionic, or negatively charged, glycosaminoglycan molecules that are similar to the chemical components of sulodexide. The glomerular filtrate, which is the precursor of what will eventually be excreted as urine, flows into the next serial component, the tubular interstitial structure. In the tubules, further water is extracted from the filtrate and minerals and other body chemicals are absorbed from or secreted into the filtrate.

In diabetic nephropathy, it is the delicate glomerular loops that first sustain damage as a result of the diabetic state. These harmful effects include:

o The delicate filtering membranes of the glomerular loops thicken and their crucial anionic glycosaminoglycan molecules are either depleted or altered and lose some or all of their negative charge. As the glycosaminoglycan negative charge provides normal filtering selectivity to the glomerular membranes, their loss of negative charge results in the release of protein, usually albumin, from the blood into the filtrate and urine. The releases of abnormal amounts of protein or albumin into the urine are called proteinuria and albuminuria, respectively.

o In addition, hyperglycemia induced overproduction of TGF beta, a regulatory protein, by the kidney induces scar forma

Show Raw Text
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<TEXT>
<PAGE>
                                 ALSTON&BIRD LLP
                                 90 Park Avenue
                            New York, New York 10016

                                  212-210-9400
                                Fax: 212-210-9444
                                 www.alston.com

Mark F. McElreath    Direct Dial: 212-210-9595     E-mail: mmcelreath@alston.com

                                 August 12, 2005

VIA: UPS AND EDGAR

Mr. Jim B. Rosenberg
Senior Assistant Chief Accountant
United States Securities and Exchange Commission
100 F Street, N.E.
Division of Corporation Finance
Mail Stop 6010
Washington, D.C. 20549

         Re:  Keryx Biopharmaceuticals, Inc.
              Annual Report on Form 10-K for the year ended December 31, 2004
              File No. 000-30929

Dear Mr. Rosenberg:

      At the request and on behalf of our client, Keryx Biopharmaceuticals, Inc.
(the "Company"), we hereby file, via EDGAR, responses to the Commission's
comment letter dated July 29, 2005, relating to the Company's Annual Report on
Form 10-K for the year ended December 31, 2004 (File No. 000-30929). These
responses have been prepared by the Company with the assistance of its legal
counsel. As requested, these responses are keyed to correspond to the
Commission's comment letter. A copy of this letter is being sent to the
Commission via overnight mail.

Comment:

Item 7. Management's Discussion and Analysis of Financial Condition and Results
 of Operations

      Please refer to the Division of Corporation Finance "Current Issues and
Rulemaking Projects Quarterly Update" under section VII - Industry Specific
Issues - Accounting and Disclosure by Companies Engaged in Research and
Development Activities. You can find it at the following website address:
http://www.sec.gov/divisions/corpfin/cfcrq032001.htm.
<TABLE>
<S>                          <C>                                  <C>                                  <C>
    One Atlantic Center             Bank of America Plaza         3201 Beechleaf Court, Suite 600      601 Pennsylvania Avenue, N.W.
1201 West Peachtree Street   101 South Tryon Street, Suite 4000       Raleigh, NC 27604-1062             North Building, 10th Floor
   Atlanta, GA 30309-3424          Charlotte, NC 28280-4000                 919-862-2200                 Washington, DC 20004-2601
       404-881-7000                     704-444-1000                     Fax: 919-862-2260                      202-756-3300
     Fax: 404-881-7777                Fax: 704-444-1111                                                      Fax: 202-756-3333
</TABLE>
<PAGE>

Page 2

Please disclose the following information for each of your major research and
development projects:

          (a)  The costs, including amounts recognized as acquired in-process
               research and development, incurred during each period presented
               and to date on the project;

          (b)  The nature, timing and estimated costs of the efforts necessary
               to complete the project;

          (c)  The anticipated completion dates; and finally

          (d)  The period in which material net cash inflows from significant
               projects are expected to commence.

      Regarding (a), please disclose the significant assumptions used in valuing
the acquired in-process research and development. If you do not maintain any
research and development costs by project, disclose that fact, explain why
management does not maintain and evaluate research and development costs by
project, and provide other quantitative or qualitative disclosure that indicates
the amount of the company's resources being used on the project.

      Regarding (b) and (c), disclose the amount or range of estimated costs and
timing to complete the phase in process and each future phase. To the extent
that information is not estimable, disclose those facts and circumstances
indicating the uncertainties that preclude you from making a reasonable
estimate.

Response:

      The Company proposes to include disclosure in the following general format
in its Annual Report on Form 10-K for the year ending December 31, 2005,
completed and updated accordingly at that time.

Response to comment (a)

      Research and development costs for the years ended December 31, 2004, 2003
and 2002 were $[_________], $[_________] and $[_________], respectively.
Research and development expenses consist primarily of salaries and related
personnel costs, fees paid to consultants and outside service providers for
clinical and laboratory development, facilities-related and other expenses
relating to the design, development, testing, and enhancement of our product
candidates and technologies, as well as expenses related to in-licensing of new
product candidates. We expense our research and development costs as they are
incurred.

      The following table sets forth the research and development costs per
project for the periods presented.
<PAGE>

Page 3

                                        Years ended December 31,
                         -------------------------------------------------------
                                                               Cumulative, as of
                                                                  of December
                            2004         2003         2002         31, 2004
                         ----------   ----------   ----------  -----------------

KRX-101.................  [______]     [______]     [______]       [______]

KRX-0401................  [______]     [______]     [______]       [______]

Other Drug Candidates...  [______]     [______]     [______]       [______]
--------------------------------------------------------------------------------
Total Research and
Development Costs.......  [______]     [______]     [______]       [______]

      As required by FASB Interpretation No. 4, "Applicability of FASB Statement
No. 2 to Business Combinations Accounted for by the Purchase Method" ("FIN 4"),
the Company recorded a non-recurring, non-cash charge in 2004 of $18,800,000 for
the portion of the purchase price of ACCESS Oncology, Inc. allocated to acquired
in-process research and development. Of the $18,800,000 charge, [__________]
relates to the portion of the purchase price allocated to KRX-0401, and the
remaining [__________] relates to the portion of the purchase price allocated to
the Company's other drug candidates acquired from ACCESS Oncology, Inc.

      A project-by-project valuation using the guidance in SFAS No. 141,
"Business Combinations" and the AICPA Practice Aid "Assets Acquired in a
Business Combination to Be Used In Research and Development Activities: A Focus
on Software, Electronic Devices and Pharmaceutical Industries" was performed
with the assistance of independent valuation specialists to determine the fair
value of research and development projects of ACCESS Oncology which were
in-process, but not yet completed.

         The fair value was determined using the income approach on a
project-by-project basis. This method starts with a forecast of the expected
future net cash flows. These cash flows are then adjusted to present value by
applying an appropriate discount rate that reflects the project's stage of
completion and other risk factors. These other risk factors can include the
nature of the product, the scientific data associated with the technology, the
current patent situation and market competition.

      The forecast of future cash flows required the following assumptions to be
made:

      o  revenue that is likely to result from specific in-process research and
         development projects, including estimated patient populations,
         estimated selling prices, estimated market penetration and estimated
         market share and year-over-year growth rates over the product life
         cycles;

      o  cost of sales related to the potential products using industry data or
         other sources of market data;
<PAGE>

Page 4

      o  sales and marketing expense using industry data or other sources of
         market data;

      o  general and administrative expenses; and

      o  research and development expenses.

      The valuations are based on information that is available as of the
acquisition date and the expectations and assumptions that have been deemed
reasonable by our management. No assurance can be given, however, that the
underlying assumptions or events associated with such assets will occur as
projected. For these reasons, among others, the actual results may vary from the
projected results.

      The Company will include the information in this response to comment (a)
in its next Annual Report on Form 10-K for the year ending December 31, 2005, in
Item 7, under a section entitled "Research and Development."

Response to comments (b) and (c)

      The Company included the information below in its Annual Report on Form
10-K for the year ended December 31, 2004, in Item 1, under a section entitled
"Products Under Development," except for the text underlined and included below.
The Company will update the information accordingly for inclusion in its Annual
Report on Form 10-K for the year ending December 31, 2005.

KRX-101

Overview

      We have obtained a license to develop sulodexide, or KRX-101, to treat
diabetic nephropathy and other conditions. Diabetic nephropathy is a long-term
complication of diabetes in which the kidneys are progressively damaged.
Sulodexide, our lead drug candidate, is a glycosaminoglycan compound with
structural similarities to the broad family of marketed heparins and low
molecular weight heparins. Specifically, sulodexide is comprised of heparan
sulfate, also referred to as fast-moving heparin, dermatan sulfate and
slow-moving heparin. This drug has been marketed in a number of European, Asian
and South American countries for many years by our licensor for certain
cardiovascular conditions and has a well established safety profile at the doses
used for such indications. Additionally, it has been demonstrated in multiple
clinical trials conducted in Europe, including a randomized, double-blind,
placebo-controlled Phase II study, that KRX-101 can reduce urinary protein
excretion in patients with diabetic nephropathy. In the fourth quarter of 2003,
we announced the initiation of our KRX-101 U.S.-based Phase II/III clinical
program for the treatment of diabetic nephropathy. In the third quarter of 2004,
we completed the target enrollment for the Phase II portion of this clinical
program. This trial is being conducted by the CSG. In January 2005, we announced
that the CSG, based
<PAGE>

Page 5

on a safety and efficacy analysis of the interim Phase II data conducted by an
independent DSMC and the CSG, respectively, recommended that we proceed to the
Phase III portion of our Phase II/III clinical program of KRX-101 for the
treatment of diabetic nephropathy, as planned.

      We plan to develop sulodexide in the United States, and possibly other
countries where we have exclusive rights under our license, for the treatment of
diabetic nephropathy and potentially for other indications.

Market Opportunity

      According to the American Diabetes Association, or ADA, there are 18.2
million people in the United States, or approximately 6.3% of the population,
who have diabetes. Of this population, approximately 13 million have been
diagnosed with the disease, of whom approximately 90-95% have been diagnosed
with diabetes mellitus, type 2, referred to as DM2. DM2 results from the
combination of insulin deficiency and the body's relative insensitivity to the
insulin present, as opposed to DM1, in which severe insulin deficiency results
from destruction of the insulin-producing beta cells of the pancreas. Moreover,
an August 2003 study published by Datamonitor estimates that approximately 50%
of all diabetics in the U.S., or approximately 9 million people, have diabetic
nephropathy. Diabetes is the most common cause of End Stage Renal Disease, or
ESRD, in the United States and in many other developed nations and represents
approximately 45% of all new cases of ESRD in the United States. Despite
advances in clinical care, including improvements in glycemic or blood sugar
control and blood pressure control, the number of DM1- and DM2-related cases of
ESRD continues to rise. In particular, the incidence of DM2-related ESRD is
rapidly increasing. Less than 20% of diabetics on dialysis in the United States
survive for five years, making the mortality of end-stage renal failure in this
group higher than most forms of cancer. Unfortunately, renal transplantation is
an option for less than 20% of diabetics with ESRD, as compared to 40-50% of
non-diabetics, principally due to age and concomitant vascular disease. Despite
recent advances, diabetic nephropathy remains a potentially catastrophic
illness, for which partial but insufficient treatment is currently available.

Scientific Background

      Both DM1 and DM2 are characterized by insufficient insulin effect upon
insulin-requiring tissues. As insulin is required for normal metabolism of
glucose, fat and protein, diabetes is accompanied by abnormal blood levels of
these substances. In the short term, hyperglycemia, or elevated blood glucose,
causes the classic symptoms of diabetes: excessive thirst, frequent urination
and weight loss. In the long term, hyperglycemia, as well as other effects
resulting from insufficient insulin effect, can progressively damage critical
anatomic structures resulting in chronic diabetic complications. We are
developing sulodexide for the treatment of diabetic nephropathy, a long-term
complication of diabetes in which the kidneys are progressively damaged. This
progressive damage results in diminished kidney function progressing to ESRD,
which ultimately leads to death unless treated by dialysis and/or renal
transplant.
<PAGE>

Page 6

      The kidney consists of two anatomically and functionally distinct
components placed in serial configuration. The first component is the
glomerulus, which performs the critical filtering function of the kidney. Blood
is passed through delicate microscopic glomerular capillary loops, which, acting
as sieves, allow waste chemicals and excess water to pass through into the
glomerular filtrate while retaining desirable components, such as blood cells
and albumin, within the blood. One of the key components of the glomerular
capillary filtering membrane is highly anionic, or negatively charged,
glycosaminoglycan molecules that are similar to the chemical components of
sulodexide. The glomerular filtrate, which is the precursor of what will
eventually be excreted as urine, flows into the next serial component, the
tubular interstitial structure. In the tubules, further water is extracted from
the filtrate and minerals and other body chemicals are absorbed from or secreted
into the filtrate.

      In diabetic nephropathy, it is the delicate glomerular loops that first
sustain damage as a result of the diabetic state. These harmful effects include:

      o  The delicate filtering membranes of the glomerular loops thicken and
         their crucial anionic glycosaminoglycan molecules are either depleted
         or altered and lose some or all of their negative charge. As the
         glycosaminoglycan negative charge provides normal filtering selectivity
         to the glomerular membranes, their loss of negative charge results in
         the release of protein, usually albumin, from the blood into the
         filtrate and urine. The releases of abnormal amounts of protein or
         albumin into the urine are called proteinuria and albuminuria,
         respectively.

      o  In addition, hyperglycemia induced overproduction of TGF beta, a
         regulatory protein, by the kidney induces scar forma