Global KRAS Inhibitor Market Outlook and Growth Opportunities 2025

KRAS inhibitors are direct, targeted anticancer agents—almost all of them low-molecular-weight small molecules—that bind oncogenic KRAS proteins and prevent them from propagating downstream signaling through the RAF–MEK–ERK and PI3K–AKT pathways. In contemporary usage the term refers to drugs that physically engage mutant KRAS itself, most commonly hotspot alleles such as KRAS G12C and increasingly G12D or multi-mutant variants, rather than to upstream or downstream pathway blockers such as EGFR, MET, MEK or ERK inhibitors that modulate the same signaling network indirectly. In practice, current approved agents are allele-selective covalent inhibitors that recognize the cysteine introduced by the G12C mutation, trap KRAS in its inactive GDP-bound conformation, and thereby attenuate the chronic proliferative and survival signaling that characterizes KRAS-mutant non-small cell lung cancer (NSCLC), colorectal cancer (CRC) and other solid tumors.

From a historical perspective KRAS inhibition represents the end of a four-decade “undruggable” saga. The RAS oncogenes HRAS and KRAS were among the first human cancer genes identified in the early 1980s, and activating RAS mutations are now known to drive roughly 20–30% of all human cancers, with KRAS the most frequently mutated isoform and almost universal in pancreatic ductal adenocarcinoma (PDAC). Despite intense medicinal-chemistry efforts, the small, smooth GTP-binding surface of KRAS was long thought to lack a druggable pocket. The field pivoted in 2013 when Shokat and colleagues described a previously unappreciated “switch II” allosteric pocket adjacent to the GTP-binding site that could be targeted by electrophilic fragments to form covalent adducts with cysteine at position 12 in KRAS G12C, opening the door to conformationally selective covalent inhibitors. This discovery set off an intense global race that, after nearly 40 years of negative experience, produced the first clinically successful KRAS-targeted drugs. Before 2021 there were no approved KRAS inhibitors and essentially no commercial revenue attributable to direct KRAS blockade; all treatment of KRAS-mutant tumors relied on cytotoxic regimens, immune checkpoint blockade, or pathway-level agents such as EGFR or MEK inhibitors.

Clinically approved G12C inhibitors share a common mechanistic architecture. Molecules such as sotorasib, adagrasib, fulzerasib, garsorasib and glecirasib exploit the nucleophilic cysteine introduced by the G12C substitution to form an irreversible covalent bond within the switch II pocket of KRAS, locking the protein in its inactive GDP-bound state and preventing productive engagement with RAF and other effectors. These drugs therefore fall into the “KRAS-OFF” category. By selectively targeting KRAS G12C, which occurs in roughly 12–14% of NSCLC and about 3–4% of CRC, they deliver precision therapy to a genetically defined minority of patients, predominantly smokers with lung adenocarcinoma and a smaller subset of patients with gastrointestinal and biliary cancers. Next-generation agents such as divarasib retain this covalent OFF-state concept but with substantially higher potency and selectivity, while emerging “KRAS-ON” or RAS(ON) tri-complex inhibitors such as daraxonrasib (RMC-6236) bind the active GTP-loaded form and are designed to cover multiple KRAS alleles rather than a single codon. In parallel, G12D-selective agents like MRTX1133 and VS-7375 are moving through early-phase trials, reflecting a broadening of the class from G12C-only to a full KRAS-mutant portfolio.

The first commercial wave of KRAS inhibitors has been defined by the U.S. and EU launches of sotorasib and adagrasib. Sotorasib (Lumakras/Lumykras, Amgen) received FDA accelerated approval on 28 May 2021 for previously treated KRAS G12C-mutated advanced or metastatic NSCLC and has since gained approvals in the EU, UK, Japan and numerous other markets for similar indications. Adagrasib (Krazati, Mirati/Bristol Myers Squibb) followed with U.S. accelerated approval in December 2022 for pretreated KRAS G12C-mutant NSCLC and subsequently secured a conditional marketing authorization in Europe in 2023–2024. In 2024 the FDA extended the class into colorectal cancer by granting accelerated approval for adagrasib plus cetuximab for previously treated KRAS G12C-mutated locally advanced or metastatic CRC, the first time a KRAS inhibitor regimen was approved in a non-lung tumor type. In January 2025, sotorasib in combination with panitumumab received FDA approval for chemorefractory KRAS G12C-mutated metastatic CRC, further cementing EGFR-targeted combinations as the backbone of G12C-directed therapy in colorectal disease.

China has rapidly built a parallel, largely domestically sourced KRAS G12C market. Fulzerasib (IBI351; Dupert®), developed by Innovent Biologics and GenFleet Therapeutics, became the first KRAS G12C inhibitor approved by the NMPA in August 2024 for previously treated advanced NSCLC and later obtained approval in Macau, giving it a cross-border commercial footprint in Greater China. Garsorasib (D-1553; Anfangning®), co-developed by InventisBio and Chia Tai Tianqing, received conditional NMPA approval in early 2025 as a Class 1 innovative drug for similar NSCLC populations, while Jacobio Pharma’s glecirasib (JAB-21822; Airuikai®) followed with approval in May 2025. Public policy has moved quickly: fulzerasib was confirmed as included in the updated National Reimbursement Drug List (NRDL) with reimbursement taking effect from 2026, and both garsorasib and glecirasib have passed national review with strong signals of broad reimbursement coverage across key lung cancer indications, effectively transforming out-of-pocket niche therapies into accessible standard options for KRAS G12C-mutant NSCLC in China. Against this backdrop, the two U.S.-originators remain largely absent from the mainland commercial market: sotorasib has received Breakthrough Therapy Designation from the Chinese CDE but no full NMPA approval, and adagrasib is only at the stage of anticipated NDA submission via partner Zai Lab. As a result, by late 2025 the global class comprises five approved KRAS G12C inhibitors—two Western and three Chinese—whose geographic segmentation sharply shapes revenue mix, competitive dynamics, and pricing references across regions.

Clinically, first-generation G12C inhibitors deliver meaningful but not transformative efficacy, with clear differences by tumor type that foreshadow both the resistance biology and the need for rational combinations. In pretreated NSCLC, sotorasib and adagrasib as monotherapy produce objective response rates in the 30–45% range with median progression-free survival of roughly 6–7 months and generally manageable toxicity, a profile that has led to their adoption as standard targeted options after failure of chemo-immunotherapy. In contrast, single-agent activity in metastatic CRC is much more modest, reflecting potent EGFR-mediated feedback re-activation of the MAPK pathway; here, the class has rapidly pivoted to combination with anti-EGFR antibodies such as cetuximab or panitumumab, which roughly doubles response rates and PFS compared with chemotherapy-based standards while keeping toxicity within the expected spectrum of diarrhea, rash and transaminase elevations. Data in PDAC and other GI malignancies remain early and mixed, constrained by extremely aggressive disease biology and high prevalence of non-G12C alleles.

Mechanisms of resistance to KRAS G12C inhibition are now well characterized and explain both the incomplete depth of response and the relatively short durability seen with monotherapy. Primary or adaptive resistance frequently involves rapid up-regulation of upstream receptor tyrosine kinases (RTKs) such as EGFR, HER2, FGFR2 or MET, leading to reactivation of RAS–MAPK signaling even in the presence of covalent G12C blockade; this mechanism is particularly prominent in CRC, where EGFR is a dominant driver. Acquired resistance after initial response can occur through on-target alterations—secondary KRAS mutations in residues within or adjacent to the switch II pocket (e.g., Y96, H95, R68), KRAS amplification, or isoform switching from KRAS G12C to other KRAS or NRAS alleles—as well as through off-target changes such as BRAF or MEK mutations, gene fusions involving ALK/RET/FGFR, PI3K pathway activation, or even histologic transformation and epithelial-to-mesenchymal transition. These resistance patterns mirror, in a more heterogeneous and multi-clonal way, the escape routes observed with EGFR or ALK TKIs, and they define the need for multi-node, allele-aware treatment strategies.

Consequently, combinatorial strategies have become the central design principle for the next phase of KRAS inhibitor development. In CRC, dual blockade of KRAS G12C and EGFR is now an approved standard: adagrasib plus cetuximab and sotorasib plus panitumumab both deliver superior PFS and response rates compared with chemotherapy in chemorefractory disease, operationalizing a “vertical inhibition” model that suppresses both upstream RTK signaling and downstream KRAS effector activation. In NSCLC, ongoing trials are testing combinations of G12C inhibitors with PD-1/PD-L1 antibodies, SHP2 inhibitors, SOS1 inhibitors, MEK or ERK inhibitors, and standard platinum doublets, aiming either to prevent resistance by blocking adaptive signaling nodes or to exploit immunogenic cell death to deepen and prolong responses. Similar principles are being extended to G12D and pan-KRAS agents, with multi-drug regimens tailored to each tumor’s co-mutational landscape (e.g., TP53, STK11, KEAP1, PTEN) and organ-specific microenvironment.

From a market-structure standpoint, the KRAS inhibitor space is still in an early diffusion phase. Only since 2021 have direct KRAS inhibitors generated meaningful commercial sales, and current revenues are heavily concentrated in a few indications—second-line KRAS G12C-mutant NSCLC and, increasingly, chemorefractory KRAS G12C-mutant CRC—across high-income health systems in North America, Europe, Japan and parts of Asia-Pacific. Penetration is constrained by the relatively low prevalence of the G12C allele compared with other KRAS mutations, mandatory companion-diagnostic testing, and the presence of competing immunotherapy-based standards of care. At the same time, the rapid entry of multiple domestic agents in China, coupled with NRDL-driven price–volume trade-offs, is setting a parallel reference curve where unit prices are lower but eligible patient volumes are large, and where payors increasingly expect head-to-head or network-meta-analytic evidence to justify premium positioning for next-generation agents with higher response rates or better brain penetration. In aggregate, the class is evolving from a single-product, single-indication niche into a diversified family of regimens segmented by allele (G12C versus G12D and others), tumor type, line of therapy and combination partner.

Looking forward, the market will be reshaped by three overlapping innovation fronts. First, more potent and selective G12C-OFF inhibitors such as divarasib and Chinese next-generation compounds are delivering response rates in the 50% range and PFS beyond 12 months in early NSCLC data, potentially displacing first-generation agents either as monotherapy or within optimized combination backbones. Second, allele-specific inhibitors for non-G12C mutations—notably G12D, which dominates PDAC and a large fraction of CRC—are moving through Phase 1/2 programs and have already shown promising preclinical and preliminary clinical activity in PDAC and NSCLC, raising the prospect that KRAS-mutant gastrointestinal cancers may finally gain true targeted options after decades of therapeutic stagnation. Third, pan-KRAS or RAS(ON) multi-selective tri-complex inhibitors such as daraxonrasib (RMC-6236) aim to cover multiple KRAS and NRAS alleles simultaneously by binding the active GTP-loaded state in cooperation with a chaperone protein, offering a conceptual route to broader patient coverage but at the expense of more complex resistance patterns and safety considerations. Together, these developments suggest that the KRAS inhibitor market will evolve over the coming decade from a narrow, G12C-centric niche into a layered ecosystem spanning G12C, G12D and multi-allelic agents, with competitive positioning determined not only by traditional efficacy–safety metrics but also by allele spectrum, central-nervous-system penetration, combinability, cost, and the ability to delay or circumvent well-characterized resistance mechanisms.

Amgen

InventisBio/Chia Tai Tianqing Pharmaceutical

Bristol Myers Squibb/Mirati

Innovent Biologics/GenFleet Therapeutics

Jacobio Pharma/Shanghai Allist Pharmaceuticals

Lung Cancer

Colorectal Cancer

Pancreatic Cancer

Others

Clinic Laboratories

Hospitals

Cancer Diagnostic Centres

Others

North America

United States

Canada

Mexico

Europe

Germany

France

U.K.

Italy

Russia

Spain

Netherlands

Switzerland

Sweden

Poland

Asia-Pacific

China

Japan

South Korea

India

Australia

Taiwan

Southeast Asia

South America

Brazil

Argentina

Chile

Colombia

Middle East & Africa

Egypt

South Africa

Israel

Türkiye

GCC Countries

Study Objectives

1. To analyze and research the global KRAS Inhibitor status and future forecast, involving, sales, revenue, growth rate (CAGR), market share, historical and forecast.

2. To present the key manufacturers, sales, revenue, market share, and Recent Developments.

3. To split the breakdown data by regions, type, manufacturers, and Application.

4. To analyze the global and key regions KRAS Inhibitor market potential and advantage, opportunity and challenge, restraints, and risks.

5. To identify KRAS Inhibitor significant trends, drivers, influence factors in global and regions.

6. To analyze KRAS Inhibitor competitive developments such as expansions, agreements, new product launches, and acquisitions in the market.

1. This report will help the readers to understand the competition within the industries and strategies for the competitive environment to enhance the potential profit. The report also focuses on the competitive landscape of the global KRAS Inhibitor market, and introduces in detail the market share, industry ranking, competitor ecosystem, market performance, new product development, operation situation, expansion, and acquisition. etc. of the main players, which helps the readers to identify the main competitors and deeply understand the competition pattern of the market.

2. This report will help stakeholders to understand the global industry status and trends of KRAS Inhibitor and provides them with information on key market drivers, restraints, challenges, and opportunities.

3. This report will help stakeholders to understand competitors better and gain more insights to strengthen their position in their businesses. The competitive landscape section includes the market share and rank (in sales and value), competitor ecosystem, new product development, expansion, and acquisition.

4. This report stays updated with novel technology integration, features, and the latest developments in the market.

5. This report helps stakeholders to gain insights into which regions to target globally.

6. This report helps stakeholders to gain insights into the end-user perception concerning the adoption of KRAS Inhibitor.

7. This report helps stakeholders to identify some of the key players in the market and understand their valuable contribution.

Chapter 1: Provides an overview of the KRAS Inhibitor market, including product definition, global market growth prospects, sales value, sales volume, and average price forecasts (2020-2031).

Chapter 2: Analysis key trends, drivers, challenges, and opportunities within the global KRAS Inhibitor industry.

Chapter 3: Detailed analysis of KRAS Inhibitor manufacturers competitive landscape, price, sales and revenue market share, latest development plan, merger, and acquisition information, etc.

Chapter 4: Provides the analysis of various market segments by type, covering the market size and development potential of each market segment, to help readers find the blue ocean market in different market segments.

Chapter 5: Provides the analysis of various market segments by application, covering the market size and development potential of each market segment, to help readers find the blue ocean market in different downstream markets.

Chapter 6: Sales and value of KRAS Inhibitor in regional level. It provides a quantitative analysis of the market size and development potential of each region and introduces the market development, future development prospects, market space, and market size of each country in the world.

Chapter 7: Sales and value of KRAS Inhibitor in country level. It provides sigmate data by type, and by application for each country/region.

Chapter 8: Provides profiles of key players, introducing the basic situation of the main companies in the market in detail, including product sales, revenue, price, gross margin, product introduction, recent development, etc.

Chapter 9: Analysis of industrial chain, including the upstream and downstream of the industry.

Chapter 10: Concluding Insights.