sutent® (sunitinib malate) slide kit

Please see full prescribing information.

SUTENT® (sunitinib malate)Slide Kit

.

Please see full prescribing information. 2

Contents

Slide

Indications 3

Dosing 4

Mechanism of Action in RCC 6

Mechanism of Action in GIST 8

SUTENT in RCC 10

SUTENT in Imatinib-Resistant or -Intolerant GIST 25

Some Strategies for Managing Adverse Reactions 40

Important Safety Information 46


SUTENT Is Approved for 2 Hard-to-Treat Tumor Types

SUTENT is indicated for the treatment of advanced renal cell carcinoma (RCC)

SUTENT is also indicated for the treatment of gastrointestinal stromal tumor (GIST) after disease progression on or intolerance to imatinib mesylate

3


SUTENT Dosing


SUTENT Efficacy and Safety Were Demonstrated Using a 50-mg Starting Dose

No dose adjustment is recommended based on age, race, gender, body weight, creatinine clearance, ECOG performance status score, or hepatic impairment (Child-Pugh Class A or B)

SUTENT dose may be easily adjusted in 12.5-mg increments


Mechanism of Action in RCC


SUTENT Inhibits Multiple Signaling Pathways Resulting in a Dual-Action Antiproliferative and Antiangiogenic Effect1

Overexpression of multiple growth factors drives RCC progression

1. Data on file. Pfizer Inc. 2. Bergers G, et al. J Clin Invest. 2003;111:1287-1295. 3. Sulzbacher I, et al. Am J Clin Pathol. 2003;120:107-112. 4. Tsuchiya N, et al. Tohoku J Exp Med. 2001;195:101-113. 5. Mendel DB, et al. Clin Cancer Res. 2003;9:327-337.

(Bergers et al2; Sulzbacher et al3; Tsuchiya et al4)

Sunitinib simultaneously inhibits all known PDGF and VEGF receptors, which play a role in both tumor cell proliferation and angiogenesis

Sunitinib induces tumor regression and inhibits angiogenesis and metastatic progression2,5

A correlation between the mechanism of action and the clinical efficacy of SUTENT has not been established.


Mechanism of Action in GIST


Sunitinib demonstrated direct antiproliferative activity by inhibiting PDGF and KIT receptorsSunitinib demonstrated antiangiogenic activity by inhibiting PDGF receptors on pericytes and VEGF receptors on endothelial cells in preclinical studies2,4

In preclinical studies, sunitinib induced tumor regression and inhibited angiogenesis andmetastatic progression

A correlation between the mechanism of action and the clinical efficacy of SUTENT has not been established.

SUTENT Inhibits Multiple Signaling Pathways

SUTENT simultaneously inhibits PDGF, VEGF, and KIT receptors for an antiproliferative and antiangiogenic effect1

1. Data on file. Pfizer Inc. 2. Bergers G, et al. J Clin Invest. 2003;111:1287-1295. 3. Heinrich MC, et al. J Clin Oncol. 2003;21:4342-4349. 4. Mendel DB, et al. Clin Cancer Res. 2003;9:327-337.

(Bergers et al2; Heinrich et al3)


SUTENT in RCC


NCCN Recommends SUTENT for 1st-Line Treatment of Metastatic Renal Cell Carcinoma (mRCC)

SUTENT has a category 1 recommendation for 1st-line treatment of patients with predominantly clear-cell mRCC regardless of MSKCC risk group1*

“…sunitinib has been given category 1 recommendation for first line treatment of patients with relapsed or medically unresectable

stage IV renal cancer with predominant clear cell and for non-clear cell histology it is a category 2A recommendation.”

—NCCN guidelines v.2.2010

NCCN = National Comprehensive Cancer Network. *Memorial Sloan-Kettering Cancer Center (MSKCC) risk groups are classified based on 5 prognostic factors that impact survival (poor performance status, high serum lactate dehydrogenase [LDH], low serum hemoglobin, high corrected serum calcium, and time from initial diagnosis to treatment). Favorable risk=0 factors; intermediate risk=1-2 factors; poor risk=≥3 factors.2

1. National Comprehensive Cancer Network®. NCCN Clinical Practice Guidelines in Oncology™. Kidney cancer. V.2.2010. 2. Motzer RJ, et al. J Clin Oncol. 2002;20:289-296.


Phase 3, Randomized, Multicenter Trial Compares SUTENT With IFN as 1st-Line Therapy in mRCC

Patient accrual ran from August 2004 through October 2005

Data were analyzed at 3 time points— First analysis: November 2005— Second analysis: June 2007— Third analysis: February 2008

Primary endpoint was progression-free survival (PFS), and secondary endpoints included objective response rate (ORR) by Response Evaluation Criteria in Solid Tumors (RECIST), overall survival (OS), patient-reported outcomes, and safety.

*Efficacy assessed by a blinded core radiology laboratory (independent assessment).

Data on file. Pfizer Inc.


Patient Baseline Characteristics WereWell Balanced Between the Arms1,2

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Totals may not equal 100% because of rounding and/or missing data. ECOG = Eastern Cooperative Oncology Group. *Data are missing for 17 patients in the IFN group.

1. Motzer RJ, et al. N Engl J Med. 2007;356:115-124. 2. Data on file. Pfizer Inc.


Patient Baseline Characteristics WereWell Balanced Between the Arms1,2 (cont’d)

Totals may not equal 100% because of rounding and/or missing data.*Data are missing for 17 patients in the IFN group.†MSKCC risk groups are classified based on 5 prognostic factors that impact survival (poor performance status, high serum LDH, low serum hemoglobin, high corrected serum calcium, and time from initial diagnosis to treatment). Favorable risk=0 factors; intermediate risk=1-2 factors; poor risk=≥3 factors.

1. Motzer RJ, et al. N Engl J Med. 2007;356:115-124. 2. Data on file. Pfizer Inc.

In both treatment arms (SUTENT and IFN):— The majority of patients were white (94% and 91%)

— Few patients had previous radiotherapy (14% and 14%)


SUTENT More Than Doubled Single-Agent Median PFS vs IFN

Median PFS was 11 months vs 5 months (with IFN)

58% reduced risk of progression or death (HR=0.42)

The median duration of treatment with SUTENT was 11 months (48 weeks) vs 4 months (18 weeks) with IFN1

1. Data on file. Pfizer Inc.

Progression-Free Survival


Median PFS Across MSKCC Risk Groups

Factors that constitute these risk groups were prespecified. The PFS efficacy analysis according to these risk factors was analyzed retrospectively. As with any retrospective analysis, there may be interpretive limitations.


Progression-Free Survival by MSKCC Risk Group

Favorable (HR=0.476;

95% Cl: 0.329, 0.688)

Intermediate (HR=0.538;

95% Cl: 0.415, 0.698)

Poor (HR=0.679;

95% Cl: 0.3305, 1.398)


SUTENT Achieved a Median OS of Single-Agent More Than 2 Years

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*Stratification factors: ECOG performance status score, LDH, and prior nephrectomy.


Overall Survival


Poststudy Treatments

18

*P<.0001.


6% of the patients in the IFN arm crossed over to SUTENT during the study; poststudy, 33% of the patients in the IFN arm received SUTENT


5-Fold Higher Objective Response Rate With SUTENT vs IFN

PR=partial response.


Objective Response Rates

Response was defined by RECIST and assessed by blinded core review at 2 different time points (November 2005 and June 2007)

(n=375) (n=375)First analysis

(n=375) (n=375)Second analysis


Treatment-Emergent ARs Reported in ≥10% of Treatment-Naïve mRCC Patients*

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*Common Terminology Criteria for Adverse Events (CTCAE), version 3.0.†Grade 4 ARs in patients on SUTENT included back pain (1%), arthralgia (<1%), asthenia (<1%), dehydration (<1%), fatigue (<1%), limb pain (<1%), and rash (<1%).

‡Grade 4 ARs in patients on IFNα included dyspnea (1%), fatigue (1%), and depression (<1%).§Includes flank pain.


Treatment-Emergent ARs Reported in ≥10% of Treatment-Naïve mRCC Patients* (cont’d)

21

*Common Terminology Criteria for Adverse Events (CTCAE), version 3.0.†Grade 4 ARs in patients on SUTENT included back pain (1%), arthralgia (<1%), asthenia (<1%), dehydration (<1%), fatigue (<1%), limb pain (<1%), and rash (<1%).

‡Grade 4 ARs in patients on IFNα included dyspnea (1%), fatigue (1%), and depression (<1%).

§Includes ageusia, hypogeusia, and dysgeusia.||Includes decreased appetite.¶ Includes one patient with grade 5 gastric hemorrhage.#Includes depressed mood.


Laboratory Abnormalities Reported in ≥10% of Treatment-Naïve mRCC Patients*

22

*Common Terminology Criteria for Adverse Events (CTCAE), version 3.0.†Grade 4 laboratory abnormalities in patients on SUTENT included uric acid (12%), lipase (3%), amylase (1%), neutrophils (1%), ALT (<1%), calcium decreased (<1%), phosphorus (<1%), potassium increased (<1%), sodium decreased (<1%), and hemoglobin (<1%).

‡Grade 4 laboratory abnormalities in patients on IFN included uric acid (8%), lipase (1%), amylase (<1%), calcium increased (<1%), glucose decreased (<1%), potassium increased (<1%), and hemoglobin (<1%).


Important Safety Information

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Women of childbearing potential should be advised of the potential hazard to the fetus and to avoid becoming pregnant.

Given the potential for serious adverse reactions in nursing infants, a decision should be made whether to discontinue nursing or SUTENT® (sunitinib malate).

Left ventricular ejection fraction declines to below the lower limit of normal have occurred. Monitor patients for signs and symptoms of congestive heart failure (CHF) and, in the presence of clinical manifestations, discontinuation is recommended. Patients who presented with cardiac events, pulmonary embolism, or cerebrovascular events within the previous 12 months were excluded from clinical studies.

SUTENT has been shown to prolong QT interval in a dose-dependent manner, which may lead to an increased risk for ventricular arrhythmias including torsades de pointes, which has been seen in <0.1% of patients. Monitoring with on-treatment electrocardiograms and electrolytes should be considered.

Hypertension may occur. Monitor blood pressure and treat as needed.


Important Safety Information (cont’d)

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There have been rare (<1%) reports of subjects with seizures and radiological evidence of reversible posterior leukoencephalopathy syndrome (RPLS). None resulted in a fatal outcome.

Hemorrhagic events including tumor-related hemorrhage have occurred. Perform serial complete blood counts (CBCs) and physical examinations.

In an ongoing clinical trial of patients with metastatic non–small cell lung cancer (NSCLC), fatal pulmonary hemorrhage occurred in 2 patients, both with squamous cell histology. SUTENT is not approved for use in patients with NSCLC.

Thyroid dysfunction may occur. Monitor thyroid function in patients with signs and/or symptoms of hypothyroidism or hyperthyroidism and treat per standard medical practice.

Adrenal hemorrhage was observed in animal studies. Monitor adrenal function in case of stress such as surgery, trauma, or severe infection.

CBCs and serum chemistries should be performed at the beginning of each treatment cycle.

Dose adjustments are recommended when administered with CYP3A4 inhibitors or inducers.


SUTENT in Imatinib-Resistant or -Intolerant GIST


Routine Monitoring and Imaging Are Essential to Identifying Disease Progression in Patients With GIST

Medical imaging is currently the best method for assessing response to therapy and detecting disease progression in patients with GIST1-4

However, assessing response using current criteria and technology can still be challenging3-5

1. Therasse P, et al. J Natl Cancer Inst. 2000;92:205-216. 2. Cancer Therapy Evaluation Program, NCI. Response Evaluation Criteria in Solid Tumors (RECIST) quick reference. 3. Choi H, et al. J Clin Oncol. 2007;25:1753-1759. 4. Demetri GD. Cancer: Principles & Practice of Oncology. 7th ed. 2004:1050-1060. 5. Blay J-Y, et al. Ann Oncol. 2005;16:566-578. 6. National Comprehensive Cancer Network®. NCCN Clinical Practice Guidelines in Oncology™. Soft tissue sarcoma. V.2.2008. 7. Phongkitkarun S, et al. World J Gastroenterol. 2008;14:892-898. 8. Benjamin RS, et al. J Clin Oncol. 2007;25:1760-1764. 9. Boyar MS, Taub RN. Cancer Invest. 2007;25:328-335.


Routine Monitoring and Imaging Are Essential to Identifying Disease Progression in Patients With GIST

Primary resistance to imatinib occurs in up to 14% of patients with GIST2-10

— Primary resistance is defined as disease progression within 6 months of imatinib treatment8,9,11-14

Secondary resistance to imatinib occurs in more than 40% of patients with GIST3,5,6,8,9,12

— Secondary resistance is defined as initial benefit from imatinib treatment followed by disease progression after 6 months and occurs after a median duration of response of 29 months and a median overall time to tumor progression of 24 months (400- and 600-mg dosing groups)11,12,15

About 5% of patients with GIST are intolerant of imatinib therapy16

When disease progression or intolerance to imatinib occurs, imatinib therapy may no longer be appropriate1

1. National Comprehensive Cancer Network®. NCCN Clinical Practice Guidelines in Oncology™. Soft tissue sarcoma. V.2.2008. 2. Boyar MS, Taub RN. Cancer Invest. 2007;25:328-335. 3. Verweij J, et al. Lancet. 2004;364:1127-1134. 4. Demetri GD, et al. N Engl J Med. 2002;347:472-480. 5. Antonescu CR, et al. Clin Cancer Res. 2005;11:4182-4190. 6. Siddiqui MA, Scott LJ. Drugs. 2007;67:805-820. 7. Sciot R, Debiec-Rychter M. Semin Diagn Pathol. 2006;23:84-90. 8. Sleijfer S, et al. Oncologist. 2007;12:719-726. 9. Van Glabbeke M, et al. J Clin Oncol. 2005;23:5795-5804. 10. Connolly EM, et al. Br J Surg. 2003;90:1178-1186. 11. Blay J-Y, et al. Ann Oncol. 2005;16:566-578. 12. Heinrich MC, et al. J Clin Oncol. 2006;24:4764-4774. 13. Badalamenti G, et al. Ann Oncol. 2007;18(suppl 6):vi136-vi140. 14. Rubin BP, Duensing A. Lab Invest. 2006;86:981-986. 15. Blanke CD, et al. J Clin Oncol. 2008;26:620-625. 16. Gleevec [package insert]. 2007.

Some patients are intolerant of or develop primary resistance to imatinib, while others may develop secondary resistance1


Understanding Primary and Secondary Mutations in GIST

Exons are genetic segments containing sequences that code for proteins, such as KIT and PDGFR1

Exon mutations can result in structurally and functionally abnormal receptors that can lead to continual (“constitutive”) activation and tumor development2,3

A primary mutation refers to a mutation that occurs prior to GIST treatment4-6

A secondary mutation refers to a mutation that occurs in addition to the primary mutation and emerges during the course of treatment4-6

1. National Institutes of Health National Human Genome Research Institute glossary. 2. Demetri GD. Cancer: Principles & Practice of Oncology. 7th ed. 2004:1050-1060. 3. National Library of Medicine. Your guide to understanding genetic conditions. 4. Antonescu CR, et al. Clin Cancer Res. 2005;11:4182-4190. 5. Heinrich MC, et al. J Clin Oncol. 2006;24:4764-4774. 6. Lasota J, Miettinen M. Histopathology. 2008;53:245-266.


Primary Mutations in KIT or PDGFR Are Common in Patients With GIST

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1. Corless CL, et al. J Clin Oncol. 2004;22:3813-3825. 2. Heinrich MC, et al. J Clin Oncol. 2003;21:4342-4349. 3. Debiec-Rychter M, et al. Eur J Cancer 2006;42:1093-1103. 4. Hopkins TG, et al. Eur J Surg Oncol. 2008;34:844-850. 5. Braconi C, et al. Ann Oncol. 2008;19:706-710. 6. Corless CL, et al. J Clin Oncol. 2005;23:5357-5364. 7. Steigen SE, et al. APMIS. 2007;115:289-298. 8. De Giorgi U, Verweij J. Mol Cancer Ther. 2005;4:495-501. 9. Antonescu CR, et al. Clin Cancer Res. 2005;11:4182-4190.


Receptor Mutations Are Common in Patients With GIST and Can Lead to the Development of Drug Resistance

Primary resistance is commonly associated with primary exon 9 mutations in patients with GIST1-5*

Secondary resistance is commonly associated with primary exon 11 mutations in patients with GIST2,3,5-8†

Secondary resistance is associated with the emergence of secondary mutations— In one study (N=43), 67% of patients who developed secondary resistance had

secondary mutations2

*Defined as disease progression within 6 months of imatinib treatment.1-4,9,10

†Defined as initial benefit from imatinib treatment followed by disease progression after 6 months and occurs after a median duration of response of 29 months and a median time to tumor progression of 24 months (400- and 600-mg dosing groups).2,9,11

1. Sleijfer S, et al. Oncologist. 2007;12:719-726. 2. Heinrich MC, et al. J Clin Oncol. 2006;24:4764-4774. 3. Badalamenti G, et al. Ann Oncol. 2007;18(suppl 6):vi136-vi140. 4. Rubin BP, Duensing A. Lab Invest. 2006;86:981-986. 5. De Giorgi U, Verweij J. Mol Cancer Ther. 2005;4:495-501. 6. Wardelmann E, et al. Clin Cancer Res. 2006;12:1743-1749. 7. Fletcher JA, Rubin BP. Curr Opin Genet Dev. 2007;17:3-7. 8. Antonescu CR, et al. Clin Cancer Res. 2005;11:4182-4190. 9. Blay J-Y, et al. Ann Oncol. 2005;16:566-578. 10. Van Glabbeke M, et al. J Clin Oncol. 2005;23:5795-5804. 11. Blanke CD, et al. J Clin Oncol. 2008;26:620-625.


Primary and Secondary Mutations Are Associated With the Development of Resistance1-6

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1. Antonescu CR, et al. Clin Cancer Res. 2005;11:4182-4190. 2. Sleijfer S, et al. Oncologist. 2007;12:719-726. 3. Heinrich MC, et al. J Clin Oncol. 2006;24:4764-4774. 4. Lasota J, Miettinen M. Histopathology. 2008;53:245-266. 5. Wardelmann E, et al. Clin Cancer Res. 2006;12:1743-1749.6. Wardelmann E, et al. Lancet Oncol. 2005;6:249-251.


*Starting dosage was 50 mg once daily, 4 weeks on/2 weeks off. Patients received SUTENT or placebo + best supportive care.


Phase 3, Randomized, Multicenter TrialEvaluated SUTENT in the Treatment ofImatinib-Resistant or -Intolerant GIST

Primary endpoint

Time to tumor progression (TTP)

Secondary endpoints

Progression-free survival

Objective response rate

Overall survival

Clinical benefit rate

Duration of response


Patient Characteristics Were Well-Balanced Between the Arms

33

*Total does not equal 100% due to rounding.†n = 205.

1. Data on file. Pfizer Inc.


4-Fold Increase in TTP and a 67% Reduced Risk of Progression

Duration of PFS was consistent with TTP

67% reduced risk of progression

Significant improvement in PFS for SUTENT (24.1 weeks [5.6 months]) vs placebo (6 weeks [1.4 months]) (hazard ratio=0.33; 95% CI: 0.24, 0.47; P<.0001)

OS data were not mature at the time of this analysis

Time to Tumor Progression


Consistent Efficacy Across Patient Subgroups

35


Risk of Progression Across Patient Subgroups

Diagnosis ≥6 months = initial diagnosis of GIST made at least 6 months prior to initiation of SUTENT.Subgroup analysis of baseline factors was evaluated using Cox proportional hazards analysis.


Treatment-Emergent ARs (≥10%) With SUTENT and More Common Than With Placebo*

36

*Common Terminology Criteria for Adverse Events (CTCAE), version 3.0.†Includes decreased appetite.

Oral pain other than mucositis/stomatitis occurred in 12 patients (6%) on SUTENT versus 3 (3%) on placebo. Hair color changes occurred in 15 patients (7%) on SUTENT versus 4 (4%) on placebo. Alopecia was observed in 10 patients (5%) on SUTENT versus 2 (2%) on placebo.


Treatment-Emergent Laboratory Abnormalities (≥10%) With SUTENT or Placebo*

37

LVEF = left ventricular ejection fraction.

*Common Terminology Criteria for Adverse Events (CTCAE), version 3.0.†Grade 4 laboratory abnormalities in patients on SUTENT included alkaline phosphatase (1%), lipase (2%), creatinine (1%), potassium decreased (1%), neutrophils (2%), hemoglobin (2%), and platelets (1%).

‡Grade 4 laboratory abnormalities in patients on placebo included amylase (1%), lipase (1%), and hemoglobin (2%).








There have been rare (<1%) reports of subjects presenting with seizures and radiological evidence of reversible posterior leukoencephalopathy syndrome (RPLS). None resulted in a fatal outcome.




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39





Some Strategies Used in Clinical Trials for Managing SUTENT Adverse Reactions


Few Patients Discontinued Therapy Due to ARs

41

*Randomized, double-blind, placebo-controlled trial of SUTENT in patients with GIST who had disease progression during prior imatinib mesylate (imatinib) treatment or who were intolerant of imatinib.


*Imatinib-resistant or -intolerant.


Patient Management Strategies for Hypertension in the SUTENT Phase 3 Clinical Trial

Hypertension may occur. Monitor blood pressure and treat as needed

Patient management strategies for hypertension included:

Incidence of severe (>200 mm Hg systolic or 110 mm Hg diastolic) hypertension— mRCC trial: SUTENT vs IFN (5% vs 1%)— GIST* trial: SUTENT vs placebo (4% vs 1%)

Incidence of hypertension— mRCC trial: SUTENT vs IFN (all grades: 30% vs 4%; grade 3/4: 10% vs <1%)— GIST* trial: SUTENT vs placebo (all grades: 15% vs 11%; grade 3/4: 4% vs 0%)


*Imatinib-resistant or -intolerant.†Recurring grade 3 toxicity requires SUTENT dose reduction.

1. Data on file. Pfizer Inc. 2. Desai J, et al. Ann Intern Med. 2006;145:660-664.

Patient Management Strategies for Hypothyroidism in the SUTENT Phase 3 Clinical Trial

Thyroid dysfunction may occur. Monitor thyroid function in patients with signs and/or symptoms of hypothyroidism or hyperthyroidism and treat per standard medical practice

Patient management strategies for hypothyroidism included:

Incidence of hypothyroidism1

— mRCC trial: SUTENT vs IFN (all grades: 3% vs <1%; no grade 3/4)— GIST* trial: SUTENT vs placebo (all grades: 4% vs 1%; grade 3/4: <1% vs 0%)

Hypothyroidism has been effectively managed2†

— All patients receiving hormone-replacement therapy effectively normalized their serum thyroid-stimulating hormone (sTSH) in a subset of patients from a phase 1/2 GIST* trial


Some Patient Management Strategiesfor Hand-Foot Syndrome

44

*Recurring grade 3 toxicity requires SUTENT dose reduction.†There is no classification of grade 4 hand-foot syndrome in the Common Terminology Criteria for Adverse Events.3

1. Data on file. Pfizer Inc. 2. American Society of Clinical Oncology (ASCO®). People Living With Cancer Web site. Managing side effects: hand-foot syndrome (palmar-plantar erythrodysesthesia). 3. Common Terminology Criteria for Adverse Events v3.0 (CTCAE). August 9, 2006.

Additional recommendations

The American Society of Clinical Oncology (ASCO®) suggests preventing or managing symptoms by2:

• Avoiding prolonged exposure of hands and feet to hot water or other heat sources• Avoiding activities that cause unnecessary force or friction on the feet• Cooling hands and feet with ice packs or cool compresses in 15- to 20-minute intervals• Elevating hands and feet when sitting or lying down• Applying mild skin-care creams

Patient management strategies for hand-foot syndrome used in the SUTENT phase 3 clinical trial included1:


Some Patient Management Strategies for Fatigue

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*Recurring grade 3 toxicity requires SUTENT dose reduction.

1. Data on file. Pfizer Inc. 2. National Comprehensive Cancer Network® (NCCN). Clinical Practice Guidelines in Oncology™. Cancer-related fatigue. V.1.2008. 3. Wood LS. Community Oncol. 2006;3:558-562.

Additional recommendations

National Comprehensive Cancer Network® (NCCN) and current literature recommend ruling out and/or treating potential underlying causes or contributing factors, including2,3:

Patient management strategies for fatigue used in the SUTENT phase 3 clinical trial included1:

• Anemia• Nutrition (anorexia, gastrointestinal problems)• Pain• Depression/emotional distress

• Sleep disturbances• Hypothyroidism• Patient activity level• Other medications (including

over-the-counter and herbal products)



46






There have been rare (<1%) reports of subjects with seizures and radiological evidence of reversible posterior leukoencephalopathy syndrome (RPLS). None resulted in a fatal outcome.









The most common ARs occurring in ≥20% of patients receiving SUTENT for treatment-naïve metastatic RCC (all grades, vs IFN) were fatigue (58% vs 55%), diarrhea (58% vs 20%), nausea (49% vs 38%), altered taste (44% vs 14%), mucositis/stomatitis (43% vs 4%), anorexia (38% vs 40%), bleeding, all sites (30% vs 8%), hypertension (30% vs 4%), vomiting (28% vs 14%), dyspepsia (28% vs 4%), rash (27% vs 11%), abdominal pain (22% vs 12%), asthenia (21% vs 24%), and hand-foot syndrome (21% vs 1%). The most common grade 3/4 ARs (occurring in ≥5% of SUTENT patients) were hypertension (10% vs <1%), fatigue (9% vs 14%), asthenia (7% vs 6%), diarrhea (6% vs 0%), and hand-foot syndrome (5% vs 0%).

The most common grade 3/4 lab abnormalities occurring in ≥8% of patients with treatment-naïve metastatic RCC receiving SUTENT (vs IFN) included lipase (16% vs 6%), uric acid (12% vs 8%), neutrophils (12% vs 7%), lymphocytes (12% vs 22%), and platelets (8% vs 0%).

The most common ARs occurring in ≥20% of patients with GIST and more commonly with SUTENT than placebo (all grades, vs placebo) were diarrhea (40% vs 27%), anorexia (33% vs 29%), skin discoloration (30% vs 23%), mucositis/stomatitis (29% vs 18%), asthenia (22% vs 11%), altered taste (21% vs 12%), and constipation (20% vs 14%). The most common grade 3/4 ARs (occurring in ≥4% of SUTENT patients) were asthenia (5% vs 3%), hand-foot syndrome (4% vs 3%), diarrhea (4% vs 0%), and hypertension (4% vs 0%).

The most common grade 3/4 lab abnormalities occurring in ≥5% of patients with GIST receiving SUTENT (vs placebo) included lipase (10% vs 7%), neutrophils (10% vs 0%), amylase (5% vs 3%), and platelets (5% vs 0%).

SUU00237BJ © 2009 Pfizer Inc. All rights reserved. October 2009


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