Exhibit 99.1

Contact:		John Beck Ardea Biosciences, Inc. (858) 652-6523 jbeck@ardeabio.com

Ardea Biosciences Announces Positive Results for RDEA594 in Combination with
Febuxostat or Allopurinol in Gout Patients

100% Response Rate Achieved with All Doses of RDEA594 Combined with Febuxostat
or Allopurinol; Serum Uric Acid Levels Reduced by Up to 80%

Company to Host Webcast at 8:30 PM Eastern Time This Evening

SAN DIEGO, November 8, 2010 — Ardea Biosciences, Inc. (Nasdaq: RDEA) today announced positive results from two clinical studies of RDEA594 in combination with currently marketed drugs for the treatment of gout patients, febuxostat (Uloric^®) and allopurinol. RDEA594, Ardea’s lead product candidate for the chronic management of hyperuricemia and gout, is an orally administered compound that inhibits the URAT1 transporter, a biological mechanism that is different from, but complementary to, that of allopurinol and febuxostat. While allopurinol and febuxostat account for greater than ninety percent of U.S. prescriptions for the chronic treatment of gout, approximately one half of patients do not adequately respond to standard doses of these drugs, leaving a significant portion of the gout population with limited options.

Combination of RDEA594 and Febuxostat (Study 111)

In this 21-patient, open-label, clinical pharmacology study, 100 percent of patients receiving the combination of RDEA594 and febuxostat achieved serum urate (or “sUA”) levels below the clinically important target of 6 mg/dL, compared to 67 percent and 56 percent for 40 mg and 80 mg, respectively, of febuxostat alone. At the highest combination doses tested (600 mg of RDEA594 and 80 mg of febuxostat), 100 percent of patients also reached sUA levels below 4 mg/dL, with 58 percent achieving levels below 3 mg/dL. No patient achieved these reduced sUA levels on either dose of febuxostat alone. The study included 2 cohorts of gout patients with sUA greater than 8 mg/dL on no urate-lowering therapy. All patients received colchicine beginning one week prior to baseline and continuing for 5 weeks for flare prophylaxis. The first cohort of patients in the study consisted of 12 gout patients with a median baseline sUA of 9.2 mg/dL who were administered 40 mg febuxostat for the first week, 40 mg febuxostat in combination with 400 mg RDEA594 for the second week, and then 40 mg febuxostat in combination with 600 mg RDEA594 for the third week. This sequence was repeated with 80 mg febuxostat in a second cohort of 9 patients who had a median baseline sUA of 10.4 mg/dL.

Cohort 1: Response Rates and Median Percent Changes from Baseline (Median Baseline
= 9.2 mg/dL) in Gout Patients for 40 mg Febuxostat Monotherapy and in Combination
with 400 mg or 600 mg RDEA594

		Febuxostat				Combination with RDEA594
		40 mg Alone				400 mg				600 mg
Response Rate (< 6 mg/dL)			67	%			100	%			100	%
Percent Patients < 4 mg/dL			0	%			50	%*			64	%**
Percent sUA Change at Trough			-35	%			-56	%***			-61	%***
Percent sUA Change Intraday			-44	%			-68	%***			-71	%***

Cohort 2: Response Rates and Median Percent Changes from Baseline (Median Baseline
= 10.4 mg/dL) in Gout Patients for 80 mg Febuxostat Monotherapy and in Combination
with 400 mg or 600 mg RDEA594

		Febuxostat				Combination with RDEA594
		80 mg Alone				400 mg				600 mg
Response Rate (< 6 mg/dL)			56	%			100	% *			100	%*
Percent Patients < 4 mg/dL			0	%			89	%***			100	%***
Percent sUA Change at Trough			-47	%			-65	%***			-73	%***
Percent sUA Change Intraday			-52	%			-78	%***			-81	%***

The combination of RDEA594 and febuxostat was synergistic, with the addition of 600 mg RDEA594 producing additional 39 and 51 percent reductions compared to 40 mg and 80 mg febuxostat alone, respectively. At the highest combination doses in cohorts one and two, patients achieved intraday median sUA levels of 2.4 mg/dL and 2.0 mg/ dL, respectively. These levels of sUA reduction suggest the combination of RDEA594 and febuxostat may be particularly useful in patients who have accumulated large deposits of uric acid, or tophi. In these patients, the substantial reduction of sUA, coupled with increased excretion of uric acid associated with RDEA594’s URAT1 mechanism, may lead to improved resolution of these tophi.

No clinically relevant drug interactions were observed between RDEA594 and febuxostat. The combination of RDEA594 and febuxostat was well tolerated, with no serious adverse events or discontinuations due to adverse events. There were no Grade 2 or higher increases in serum creatinine on RDEA594 alone or the combination with febuxostat, but one Grade 2 serum creatinine increase occurred on colchicine alone. There was one Grade 3 increase in the liver enzyme, alanine aminotransferase (ALT), on febuxostat 40 mg alone, which normalized during combination treatment with RDEA594.

Combination of RDEA594 and Allopurinol (Study 110)

In this 20-patient, open-label clinical pharmacology study, 100 percent of patients receiving all combinations of RDEA594 and allopurinol achieved sUA reductions to below the 6 mg/dL target. On 300 mg allopurinol alone, only 20 percent of patients achieved target sUA levels below 6 mg/dL. On 600 mg RDEA594 alone, 67 percent of patients achieved sUA levels below 6 mg/dL, which was significantly better than allopurinol alone (p <0.05). At the highest combination doses tested, 90 percent of patients also reached sUA levels below 5 mg/dL, and 50 percent reached levels below 4 mg/dL. Study 110’s design was similar, but not identical, to Study 111 and included 2 cohorts of gout patients with sUA greater than 8 mg/dL on no urate-lowering therapy who began colchicine dosing one week prior to baseline and continued it for 5 weeks. In this study, the first cohort of 10 patients with a median baseline sUA of 9.8 mg/dL received 300 mg allopurinol alone for the first week, then 300 mg allopurinol plus 400 mg RDEA594 for the second week, followed by 400 mg RDEA594 alone for the third week. In the second cohort, 10 patients with a median baseline sUA of 9.1 mg/dL followed the same dosing scheme for the same time period at a dose of 300 mg allopurinol and 600 mg RDEA594.

Cohort 1: Response Rates and Median Percent Changes from Baseline (Median Baseline
= 9.8 mg/dL) in Gout Patients for 300 mg Allopurinol Monotherapy, Allopurinol
Combination with 400 mg RDEA594, and 400 mg RDEA594 Monotherapy

		Allopurinol				Combination with				RDEA594
		300 mg Alone				RDEA594 400 mg				400 mg Alone
Response Rate (< 6 mg/dL)			10	%			100	%***			20	%
Percent Patients < 5 mg/dL			5	%			50	%**			0	%
Percent sUA Change at Trough			-31	%			-45	%***			-28	%
Percent sUA Change Intraday			-38	%			-62	%***			-44	%*

Cohort 2: Response Rates and Median Percent Changes from Baseline (Median Baseline
= 9.1 mg/dL) in Gout Patients for 300 mg Allopurinol Monotherapy, Allopurinol
Combination with 600 mg RDEA594, and 600 mg RDEA594 Monotherapy

		Allopurinol				Combination with				RDEA594
		300 mg Alone				RDEA594 600 mg				600 mg Alone
Response Rate (< 6 mg/dL)			30	%			100	%***			67	%*
Percent Patients < 5 mg/dL			5	%			90	%***			33	%
Percent sUA Change at Trough			-27	%			-55	%***			-39	%**
Percent sUA Change Intraday			-35	%			-70	%***			-54	%***

At the highest combination doses tested, intraday median sUA levels below 3 mg/dL were achieved. No clinically relevant drug interactions were observed between RDEA594 and allopurinol in this study; however, consistent with prior experience, plasma levels of oxypurinol, an active metabolite of allopurinol, were decreased approximately 25-35 percent. Despite this small decrease, the combination of 600 mg RDEA594 and allopurinol demonstrated a completely additive response.

The combination of RDEA594 and allopurinol was well tolerated. There were no serious adverse events or discontinuations that were considered possibly related to RDEA594 or the combination. There were no clinically relevant increases in serum creatinine or ALT in this study. Two patients receiving RDEA594 and colchicine had Grade 4 increases in creatine kinase (CK); one of these, although asymptomatic, was considered to be rhabdomyolysis by the investigator. Both cases were considered possibly related to colchicine and not related to RDEA594. Elevations in CK and rhabdomyolysis are known side effects of colchicine. One of these patients was also receiving a statin, which is also known to cause CK elevations, particularly when combined with colchicine. Clinically significant elevations in CK have not been observed in more than 400 patients exposed to RDEA594 who were not also receiving colchicine. Furthermore, in a previously reported, randomized, monotherapy, placebo-controlled trial (Study 202), the rate of Grade 4 CK increases was lower in patients receiving RDEA594 plus colchicine (2 percent) than those receiving colchicine alone (4 percent).

“We are very pleased with these results, which demonstrate the ability of RDEA594 in combination with current standard of care to reduce uric acid levels in gout patients to an extent generally only achieved with intravenous therapy,” commented Barry D. Quart, PharmD, Ardea’s president and chief executive officer. “Based on these results, we are well-positioned to conduct further studies of these well-tolerated oral combinations in patients with the most severe forms of gout.”

Webcast – Monday, November 8, 2010 at 8:30 p.m.

Ardea will host a live webcast on Monday, November 8, 2010 from 8:30 p.m. to 9:30 p.m. Eastern Standard Time. To access the webcast, please log onto Ardea’s website at www.ardeabio.com and click on the Investors Relations section approximately 10 minutes prior to the start of the webcast to allow for any software downloads that may be necessary. An archived recording of the event will be available on Ardea’s website for one month.

About Hyperuricemia and Gout

Gout is a painful, debilitating and progressive disease caused by abnormally elevated levels of uric acid in the blood stream. This leads to the deposition of painful, needle-like uric acid crystals

in and around the connective tissue of the joints and in the kidneys, resulting in inflammation, the formation of disfiguring nodules (tophi), intermittent attacks of severe pain (acute flares) and kidney damage (nephropathy). In addition, evidence suggests that the chronic elevation of uric acid associated with gout, known as hyperuricemia, may also have systemic consequences, including an increased risk for kidney dysfunction and cardiovascular disease.

In 2008, approximately 8.3 million patients in the U.S., 6.4 million patients in the European Union and 2.9 million patients in Japan were diagnosed with gout. Gout is the most common form of inflammatory arthritis in men over the age of 40 and represents a significant unmet medical need with limited treatment options.

About RDEA594

Our most advanced product candidate for the treatment of hyperuricemia and gout, RDEA594, is an oral, once-daily inhibitor of URAT1, a transporter in the kidney that regulates uric acid excretion from the body. Approximately 90% of gout patients are considered to be under-excretors of uric acid, and recent studies have shown that defects in renal transporters have been genetically linked to gout. Consequently, increasing renal excretion of uric acid by moderating URAT1 transporter activity may provide the most physiologically appropriate treatment for gout. In addition, because increasing the excretion of serum uric acid is additive to the effects of drugs such as allopurinol that decrease the production of uric acid, RDEA594 in combination with such drugs has the potential to treat the significant portion of the gout population that is not adequately treated with existing therapies.

RDEA594 is in Phase 2 development as a single agent and in combination with the approved xanthine oxidase inhibitor, allopurinol. Over 500 people have received RDEA594 in Phase 1 and 2 clinical trials.

About Ardea Biosciences, Inc.

Ardea Biosciences, Inc., of San Diego, California, is a biotechnology company focused on the development of small-molecule therapeutics for the treatment of serious diseases. RDEA594, our lead product candidate for the treatment of hyperuricemia and gout, is a selective URAT1 transporter inhibitor in Phase 2 clinical development. Our next-generation URAT1 inhibitor program is currently in preclinical development. BAY 86-9766, formerly known as RDEA119, is a potent and specific inhibitor of mitogen-activated ERK kinase (MEK) for the treatment of cancer being developed under a global license agreement with Bayer HealthCare AG. BAY 86-9766 has been evaluated in advanced cancer patients with different tumor types as a single agent in a Phase 1 study and is currently being evaluated in combination with sorafenib (Nexavar^®; Bayer HealthCare, Onyx Pharmaceuticals) in a Phase 1/2 study. Our two product candidates for the treatment of HIV, RDEA806 and RDEA427, are non-nucleoside reverse transcriptase inhibitors (NNRTIs), which have successfully completed a Phase 2a study in HIV patients and a human micro-dose pharmacokinetic study in healthy volunteers, respectively.

Statements contained in this press release regarding matters that are not historical facts are “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. Such statements include, but are not limited to, statements regarding our plans and goals, the expected properties and benefits of RDEA594, BAY 86-9766 (RDEA119), RDEA806, RDEA427 and our other compounds and the timing and results of our preclinical, clinical and other studies. Risks that contribute to the uncertain nature of the forward-looking statements include risks related to the outcome of preclinical and clinical studies, risks related to regulatory approvals, delays in commencement of preclinical and clinical studies, costs associated with our drug discovery and

development programs, and risks related to the outcome of our business development activities, including collaboration or license agreements. These and other risks and uncertainties are described more fully in our most recently filed SEC documents, including our Annual Report on Form 10-K and our Quarterly Reports on Form 10-Q, under the headings “Risk Factors.” All forward-looking statements contained in this press release speak only as of the date on which they were made. We undertake no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made.

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