Resistance in GIST warrants a different therapeutic approach1

Advanced GIST is a highly complex disease with a myriad of mutations fueling resistance and progression1,2

GIST is often driven by primary, activating mutations in kinase genes.3

  • These mutations keep the kinase in the active state, causing uncontrolled cell proliferation and/or cell survival4,5
Molecular Classification of GIST3,6,7
Gene/exon Primary
mutation
frequency		 Secondary
mutation
frequency
KIT 70-80%
  Exon 9 10%
  Exon 11 60-70%
  Exon 13 1% 56%
  Exon 17 1% 41%
PDGFRA 5-10%
  Exon 12 1%
  Exon 14 <1%
  Exon 18 (D842V and other) 6% 3%
Wild type
SDH Deficient, NF-1, BRAF		 10-15%
 

Advanced GIST is marked by the development of secondary, drug-resistant mutations, which play a key role in disease progression2,3,8

  • Broad inter- and intra-tumor heterogeneity exists among secondary resistance mutations

A single patient with GIST may have multiple mutations WITHIN or BETWEEN tumors1,9

  Primary lesion

  Secondary lesion

For illustrative purposes

GIST mutations shown in multiple locations in the body

The majority of advanced GIST patients will eventually develop
resistance, and require lifelong TKI therapy10

As resistance develops, treatments may lose their ability to control disease progression

  • The vast majority of patients who benefit from front-line TKI therapy will eventually develop resistance2,3
  • As secondary resistance mutations emerge, some TKIs may lose their ability to prevent kinase activation, leading to cancer cell proliferation6,9,11

Currently there are several therapies for advanced GIST patients, yet some patients still do not receive all treatments they are eligible for

Life‑long systemic therapy is recommended by the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for TKI‑sensitive recurrent or metastatic GIST12

Clinical experience suggests that discontinuing TKI therapy, even in the
setting of progressive disease, may accelerate the pace of disease progression and worsen symptoms12

Median PFS and ORR13-16

Figure depicting FDA-approved lines of therapy in advanced GIST and highlighting unmet need that only 50% of first-line patients make it through to be eligible for fourth-line treatment Figure depicting FDA-approved lines of therapy in advanced GIST and highlighting unmet need that only 50% of first-line patients make it through to be eligible for fourth-line treatment


  • The FDA-approved 1st-, 2nd-, and 3rd-line therapies for GIST are imatinib, sunitinib, and regorafenib, respectively14-16
  • Avapritinib is approved for patients with unresectable or metastatic GIST harboring a PDGFRA exon 18 mutation (5–6% of patients), irrespective of line of therapy3,17

*PFS converted from weeks to months.

† Excludes estimated proportion of patients who are not eligible for treatment due to death, discontinuation of oncology treatment, or clinical trial enrollment based on recent analyses of US claims data.


A padlock

Qinlock is engineered to block the drivers of resistance in advanced GIST11,18

Qinlock is the first and only switch-control kinase inhibitor that broadly inhibited KIT and PDGFRA kinase signaling in preclinical studies11,18

Learn about
the MOA
A line graph showing two decreasing lines

Powerful PFS Results

Qinlock significantly improved PFS vs placebo (6.3 months vs 1.0 month; P<0.0001)18

See The Data
A group of people

Robust Phase 3 Trial

The efficacy and safety of Qinlock was demonstrated in the INVICTUS trial18

Invictus Study Design
A customer service agent wearing a headset

Patient Support

Learn about the services available to help patients start Qinlock

Access Assistance

1L=1st‑line; BRAF=B‑Raf proto‑oncogene, serine/threonine kinase; FDA=Food and Drug Administration; GIST=gastrointestinal stromal tumor; KIT=KIT proto‑oncogene receptor tyrosine kinase; mPFS=median progression‑free survival; MOA=mechanism of action; NCCN=National Comprehensive Cancer Network®; NF‑1=neurofibromatosis type 1; ORR=objective response rate; PDGFRA=platelet‑derived growth factor receptor alpha; SDH=succinate dehydrogenase; TKI=tyrosine kinase inhibitor.

References: 1. Ordog T, Zörnig M, Hayashi Y. Targeting disease persistence in gastrointestinal stromal tumors. Stem Cells Transl Med. 2015;4(7):702‑707. 2. Antonescu CR, DeMatteo RP. CCR 20th Anniversary commentary: a genetic mechanism of imatinib resistance in gastrointestinal stromal tumor—where are we a decade later? Clin Cancer Res. 2015;21(15):3363‑3365. 3. Lopes LF, Bacchi CE. Imatinib treatment for gastrointestinal stromal tumor (GIST). J Cell Mol Med. 2010;14(1‑2):42‑50. 4. Gramza AW, Corless CL, Heinrich MC. Resistance to tyrosine kinase inhibitors in gastrointestinal stromal tumors. Clin Care Res. 2009;15(24):7510‑7518. 5. Yan W, Zhang A, Powell MJ. Genetic alteration and mutation profiling of circulating cell‑free tumor DNA (cfDNA) for diagnosis and targeted therapy of gastrointestinal stromal tumors. Chin J Cancer. 2016;35:68. 6. Hemming ML, Heinrich MC, Bauer S, George S. Translational insights into gastrointestinal stromal tumor and current clinical advances. Ann Oncol. 2018;29(10):2037‑2045. 7. Heinrich MC, Maki RG, Corless CL, et al. Primary and secondary kinase genotypes correlate with the biological and clinical activity of sunitinib in imatinib-resistant gastrointestinal stromal tumor. J Clin Oncol. 2008;26(33):5352‑5359. 8. Zhao X, Yue C. Gastrointestinal stromal tumor. J Gastrointest Oncol. 2012;3(3):189‑208. 9. Li K, Cheng H, Li Z, et al. Genetic progression in gastrointestinal stromal tumors: mechanisms and molecular interventions. Oncotarget. 2017;8(36):60589‑60604. 10. Duffaud F, Le Cesne A. Recent advances in managing gastrointestinal stromal tumor. F1000Res. 2017;6(F1000 Faculty Rev):1689. 11. Smith BD, Kaufman MD, Lu WP, et al. Ripretinib (DCC‑2618) is a switch control kinase inhibitor of a broad spectrum of oncogenic and drug‑resistant KIT and PDGFRA variants. Cancer Cell. 2019;35(5):738‑751. 12. Referenced with permission from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for Gastrointestinal Stromal Tumors (GIST) V.1.2025. © National Comprehensive Cancer Network, Inc. 2025. All rights reserved. Accessed June 10, 2025. To view the most recent and complete version of the guideline, go online to NCCN.org. NCCN makes no warranties of any kind whatsoever regarding their content, use or application and disclaims any responsibility for their application or use in any way. 13. Demetri GD, Reichardt P, Kang YK, et al. Efficacy and safety of regorafenib for advanced gastrointestinal stromal tumours after failure of imatinib and sunitinib: an international, multicentre, prospective, randomised, placebo‑controlled phase 3 trial (GRID). Lancet. 2013;381(9863):295‑302. 14. Sutent [package insert]. New York, NY: Pfizer Inc; 2020. 15. Stivarga [package insert]. Whippany, NJ: Bayer HealthCare Pharmaceuticals Inc; 2020. 16. Gleevec [package insert]. East Hanover, NJ: Novartis Pharmaceuticals Corp; 2024. 17. Ayvakit [package insert]. Cambridge, MA: Blueprint Medicines Corp; 2020. 18. Qinlock [package insert]. Waltham, MA: Deciphera Pharmaceuticals, LLC. 19. Data on file. Deciphera Pharmaceuticals, LLC; 2020. 20. Blay JY, Serrano C, Heinrich MC, et al. Ripretinib in patients with advanced gastrointestinal stromal tumours (INVICTUS): a double-blind, randomised, placebo-controlled, phase 3 trial. Lancet Oncol. 2020;21(7):923‑934. 21. Brackert S, Polson K. Management of patients with advanced gastrointestinal stromal tumor: emphasis on fourth-line treatment with ripretinib. J Adv Pract Oncol. 2023;14(4):317‑328. 22. Tetzlaff ED, Davey MP. Optimizing adherence to adjuvant imatinib in gastrointestinal stromal tumor. J Adv Pract Oncol. 2013;4(4):238‑50.

Indication & Important Safety Info

Indication

Qinlock is a kinase inhibitor indicated for the treatment of adult patients with advanced gastrointestinal stromal tumor (GIST) who have received prior treatment with 3 or more kinase inhibitors, including imatinib.

Important Safety Information

There are no contraindications for Qinlock.

Palmar‑plantar erythrodysesthesia syndrome (PPES): In INVICTUS, Grade 1–2 PPES occurred in 21% of the 85 patients who received Qinlock. PPES led to dose discontinuation in 1.2% of patients, dose interruption in 2.4% of patients, and dose reduction in 1.2% of patients. Based on severity, withhold Qinlock and then resume at same or reduced dose.

New Primary Cutaneous Malignancies: In INVICTUS, cutaneous squamous cell carcinoma (cuSCC) occurred in 4.7% of the 85 patients who received Qinlock with a median time to event of 4.6 months (range 3.8 to 6 months). In the pooled safety population, cuSCC and keratoacanthoma occurred in 7% and 1.9% of patients, respectively. In INVICTUS, melanoma occurred in 2.4% of the 85 patients who received Qinlock. In the pooled safety population, melanoma occurred in 0.9% of patients. Perform dermatologic evaluations when initiating Qinlock and routinely during treatment. Manage suspicious skin lesions with excision and dermatopathologic evaluation. Continue Qinlock at the same dose.

Hypertension: In INVICTUS, Grade 1–3 hypertension occurred in 14% of the 85 patients who received Qinlock, including Grade 3 hypertension in 7% of patients. Do not initiate Qinlock in patients with uncontrolled hypertension. Monitor blood pressure as clinically indicated. Based on severity, withhold Qinlock and then resume at same or reduced dose or permanently discontinue.

Cardiac Dysfunction: In INVICTUS, cardiac failure occurred in 1.2% of the 85 patients who received Qinlock. In the pooled safety population, cardiac dysfunction (including cardiac failure, acute left ventricular failure, diastolic dysfunction, and ventricular hypertrophy) occurred in 1.7% of patients, including Grade 3 adverse reactions in 1.1% of patients.

In INVICTUS, Grade 3 decreased ejection fraction occurred in 1.3% of the 77 patients who received Qinlock and who had a baseline and at least one post‑baseline echocardiogram. In the pooled safety population, Grade 3 decreased ejection fraction occurred in 1.9% of the 263 patients who received Qinlock and who had a baseline and at least one post‑baseline echocardiogram.

In INVICTUS, cardiac dysfunction led to dose discontinuation in 1.2% of the 85 patients who received Qinlock. The safety of Qinlock has not been assessed in patients with a baseline ejection fraction below 50%. Assess ejection fraction by echocardiogram or MUGA scan prior to initiating Qinlock and during treatment, as clinically indicated. Permanently discontinue Qinlock for Grade 3 or 4 left ventricular systolic dysfunction.

Risk of Impaired Wound Healing: Qinlock has the potential to adversely affect wound healing. Withhold Qinlock for at least 1 week prior to elective surgery. Do not administer for at least 2 weeks following major surgery and until adequate wound healing. The safety of resumption of Qinlock after resolution of wound healing complications has not been established.

Photosensitivity: Qinlock may cause photosensitivity reactions. In 621 patients treated with Qinlock in clinical trials, photosensitivity reactions occurred in 0.6% of patients. Advise patients to limit direct ultraviolet exposure during treatment with Qinlock and for at least 1 week after discontinuation of treatment.

Embryo‑Fetal Toxicity: Qinlock can cause fetal harm when administered to a pregnant woman. Advise pregnant women of the potential risk to a fetus. Advise females of reproductive potential and males with female partners of reproductive potential to use effective contraception during treatment and for 1 week after the last dose. Because of the potential for serious adverse reactions in the breastfed child, advise women not to breastfeed during treatment and for 1 week after the last dose. Qinlock may impair fertility in males of reproductive potential.

Adverse Reactions: The most common adverse reactions (≥20%) were alopecia, fatigue, nausea, abdominal pain, constipation, myalgia, diarrhea, decreased appetite, PPES, and vomiting. The most common Grade 3 or 4 laboratory abnormalities (≥4%) were increased lipase and decreased phosphate.

The safety and effectiveness of Qinlock in pediatric patients have not been established.

Administer strong CYP3A inhibitors with caution. Monitor patients who are administered strong CYP3A inhibitors more frequently for adverse reactions. Avoid concomitant use with strong and moderate CYP3A inducers. If a moderate CYP3A inducer cannot be avoided, increase Qinlock dosing frequency from the recommended dose of 150 mg once daily to 150 mg twice daily during the co‑administration period. If the concomitant moderate CYP3A inducer is discontinued, resume Qinlock dosage back to 150 mg once daily 14 days after the discontinuation of the moderate CYP3A inducer.

Please see full Prescribing Information, including Patient Information.

To report SUSPECTED ADVERSE REACTIONS, contact Deciphera Pharmaceuticals, LLC, at 1-888-724-3274 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.

Indication & Important Safety Info

Indication

Qinlock is a kinase inhibitor indicated for the treatment of adult patients with advanced gastrointestinal stromal tumor (GIST) who have received prior treatment with 3 or more kinase inhibitors, including imatinib.

Important Safety Information

There are no contraindications for Qinlock.

Palmar‑plantar erythrodysesthesia syndrome (PPES): In INVICTUS, Grade 1–2 PPES occurred in 21% of the 85 patients who received Qinlock. PPES led to dose discontinuation in 1.2% of patients, dose interruption in 2.4% of patients, and dose reduction in 1.2% of patients. Based on severity, withhold Qinlock and then resume at same or reduced dose.

New Primary Cutaneous Malignancies: In INVICTUS, cutaneous squamous cell carcinoma (cuSCC) occurred in 4.7% of the 85 patients who received Qinlock with a median time to event of 4.6 months (range 3.8 to 6 months). In the pooled safety population, cuSCC and keratoacanthoma occurred in 7% and 1.9% of patients, respectively. In INVICTUS, melanoma occurred in 2.4% of the 85 patients who received Qinlock. In the pooled safety population, melanoma occurred in 0.9% of patients. Perform dermatologic evaluations when initiating Qinlock and routinely during treatment. Manage suspicious skin lesions with excision and dermatopathologic evaluation. Continue Qinlock at the same dose.

Hypertension: In INVICTUS, Grade 1–3 hypertension occurred in 14% of the 85 patients who received Qinlock, including Grade 3 hypertension in 7% of patients. Do not initiate Qinlock in patients with uncontrolled hypertension. Monitor blood pressure as clinically indicated. Based on severity, withhold Qinlock and then resume at same or reduced dose or permanently discontinue.

Cardiac Dysfunction: In INVICTUS, cardiac failure occurred in 1.2% of the 85 patients who received Qinlock. In the pooled safety population, cardiac dysfunction (including cardiac failure, acute left ventricular failure, diastolic dysfunction, and ventricular hypertrophy) occurred in 1.7% of patients, including Grade 3 adverse reactions in 1.1% of patients.

In INVICTUS, Grade 3 decreased ejection fraction occurred in 1.3% of the 77 patients who received Qinlock and who had a baseline and at least one post‑baseline echocardiogram. In the pooled safety population, Grade 3 decreased ejection fraction occurred in 1.9% of the 263 patients who received Qinlock and who had a baseline and at least one post‑baseline echocardiogram.

In INVICTUS, cardiac dysfunction led to dose discontinuation in 1.2% of the 85 patients who received Qinlock. The safety of Qinlock has not been assessed in patients with a baseline ejection fraction below 50%. Assess ejection fraction by echocardiogram or MUGA scan prior to initiating Qinlock and during treatment, as clinically indicated. Permanently discontinue Qinlock for Grade 3 or 4 left ventricular systolic dysfunction.

Risk of Impaired Wound Healing: Qinlock has the potential to adversely affect wound healing. Withhold Qinlock for at least 1 week prior to elective surgery. Do not administer for at least 2 weeks following major surgery and until adequate wound healing. The safety of resumption of Qinlock after resolution of wound healing complications has not been established.

Photosensitivity: Qinlock may cause photosensitivity reactions. In 621 patients treated with Qinlock in clinical trials, photosensitivity reactions occurred in 0.6% of patients. Advise patients to limit direct ultraviolet exposure during treatment with Qinlock and for at least 1 week after discontinuation of treatment.

Embryo‑Fetal Toxicity: Qinlock can cause fetal harm when administered to a pregnant woman. Advise pregnant women of the potential risk to a fetus. Advise females of reproductive potential and males with female partners of reproductive potential to use effective contraception during treatment and for 1 week after the last dose. Because of the potential for serious adverse reactions in the breastfed child, advise women not to breastfeed during treatment and for 1 week after the last dose. Qinlock may impair fertility in males of reproductive potential.

Adverse Reactions: The most common adverse reactions (≥20%) were alopecia, fatigue, nausea, abdominal pain, constipation, myalgia, diarrhea, decreased appetite, PPES, and vomiting. The most common Grade 3 or 4 laboratory abnormalities (≥4%) were increased lipase and decreased phosphate.

The safety and effectiveness of Qinlock in pediatric patients have not been established.

Administer strong CYP3A inhibitors with caution. Monitor patients who are administered strong CYP3A inhibitors more frequently for adverse reactions. Avoid concomitant use with strong and moderate CYP3A inducers. If a moderate CYP3A inducer cannot be avoided, increase Qinlock dosing frequency from the recommended dose of 150 mg once daily to 150 mg twice daily during the co‑administration period. If the concomitant moderate CYP3A inducer is discontinued, resume Qinlock dosage back to 150 mg once daily 14 days after the discontinuation of the moderate CYP3A inducer.

Please see full Prescribing Information, including Patient Information.

To report SUSPECTED ADVERSE REACTIONS, contact Deciphera Pharmaceuticals, LLC, at 1-888-724-3274 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.