C4 Therapeutics Presents New Preclinical Data for CFT1946 Highlighting Superior Activity as a Single Agent to Clinically Approved BRAF Inhibitor Standard of Care Combinations at the American Association for Cancer Research Annual Meeting 2024

On April 8, 2024 C4 Therapeutics, Inc. (C4T) (Nasdaq: CCCC), a clinical-stage biopharmaceutical company dedicated to advancing targeted protein degradation science, reported a poster today at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2024 highlighting new preclinical data for CFT1946 across multiple models of BRAF V600X mutant colorectal cancer (CRC) and non-small cell lung cancer (NSCLC), additional BRAF inhibitor (BRAFi)-resistant melanoma models, and an intracranial model of BRAF V600E metastatic melanoma (Press release, C4 Therapeutics, APR 8, 2024, View Source [SID1234641857]).

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

CFT1946 is an orally bioavailable BiDAC degrader that selectively degrades the BRAF V600X mutant protein and prevents RAF dimer-mediated resistance. While currently approved BRAF inhibitors are also selective for BRAF V600X mutant proteins, their activity is limited by primary or acquired resistance often mediated by mechanisms that promote RAF dimerization. Further, in a significant number of patients with BRAF V600X melanoma and NSCLC, the disease metastasizes to the brain. BRAF inhibitors have limited brain penetration, while CFT1946 demonstrates CNS activity in preclinical models.

Key findings include:

Promising activity of CFT1946 as a single agent in a broad range of BRAF V600X preclinical models, including models of BRAFi resistance.
CFT1946 as a single agent and in combination with cetuximab demonstrates superior activity to the standard of care combination, BRAFi with cetuximab, in all CRC models tested to date, further supporting the potential of a degrader advantage in this setting.
CFT1946 demonstrates superior prolongation of survival when compared to encorafenib in an intracranial model of metastatic melanoma.
Collectively, these data support the ongoing clinical evaluation of CFT1946, which is the only BRAF V600X degrader in the clinic to date. The CFT1946 Phase 1/2 trial continues to progress and data from the Phase 1 monotherapy dose escalation portion of the trial are expected to be presented in the second half of this year.

Details of the poster are as follows:

Title: CFT1946, a potent, selective BRAF V600X mutant-specific degrader demonstrates superior activity as a single agent to clinically approved BRAF inhibitors and standard of care combinations in preclinical models of BRAF V600X melanoma, CRC, NSCLC, and brain metastasis
Abstract Number: 1658
Session Date and Time: Monday April 8, 2024 9:00 AM – 12:30 PM PT
Location: Poster Section 14
Session Title: Cell Signaling Components as Therapeutic Targets
Presenter: Bridget Kreger, Ph.D., principal scientist, biology

The poster will be made available after the presentation under the scientific presentations and publications page of the company’s website at www.c4therapeutics.com.

KRAZATI (adagrasib) in Combination with Cetuximab Demonstrates Clinically Meaningful Activity as a Targeted Treatment Option for Patients with Previously Treated KRAS G12C-Mutated Locally Advanced or Metastatic Colorectal Cancer (CRC)

On April 8, 2024 Bristol Myers Squibb (NYSE: BMY) reported data from the cohorts of the Phase 1/ 2 KRYSTAL-1 study evaluating KRAZATI (adagrasib) in combination with cetuximab for the treatment of patients with previously treated KRASG12C-mutated locally advanced or metastatic colorectal cancer (CRC) (Press release, Bristol-Myers Squibb, APR 8, 2024, View Source [SID1234641856]).

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

These late breaking data (abstract #CT013) will be featured in an oral presentation at the 2024 American Association for Cancer Research (AACR) (Free AACR Whitepaper) annual meeting on Monday, April 8 at 11:10 a.m. Pacific Time and will be highlighted as part of the meeting’s official press program. The data will also be published simultaneously in Cancer Discovery .

With a median follow up of 11.9 months in 94 patients, KRAZATI plus cetuximab demonstrated an objective response rate, the primary endpoint, of 34%, median progression-free survival of 6.9 months (95% CI, 5.7-7.4), and median overall survival of 15.9 months (95% CI, 11.8-18.8) in pre-treated patients with KRASG12C-mutated locally advanced or metastatic CRC. The median duration of response was 5.8 months. Disease control was observed in 85% of patients. The safety profile for KRAZATI plus cetuximab was manageable and consistent with previous reports, and with the known safety profile of each drug individually.

KRASG12C mutations act as oncogenic drivers and occur in approximately 3-4% of colorectal cancers. In previous studies, treatment with cetuximab as a single agent did not offer a clinical benefit in patients with KRAS-mutated colorectal cancer.

"Patients with KRASG12C-mutated colorectal cancer have historically faced poor prognoses and remain in need of additional treatment options," said Scott Kopetz, M.D., Ph.D, FACP, associate vice president for translational research, and Professor, Department of Gastrointestinal Medical Oncology at The University of Texas MD Anderson Cancer Center. "Although KRAS had previously been considered ‘undruggable,’ these data from KRYSTAL-1 reinforce the potential benefit of adagrasib for these specific patients."

"While there has been progress in the treatment of colorectal cancer, there remain groups of patients, such as those with KRAS-mutated cancers, who continue to need new, targeted treatment options," said Anne Kerber, senior vice president, head of late clinical development, Hematology, Oncology, Cell Therapy (HOCT) at Bristol Myers Squibb. "These data highlight the significance of testing and identification of KRASG12C mutations in patients with CRC."

The company announced in February 2024 that the FDA had accepted a supplemental new drug application for KRAZATI in combination with cetuximab as a targeted treatment option for patients with previously treated KRASG12C-mutated locally advanced or metastatic CRC for priority review and assigned a Prescription Drug User Fee Act (PDUFA) goal date of June 21, 2024.

Bristol Myers Squibb thanks the patients and investigators involved in the KRYSTAL-1 clinical trial.

This study was funded by Mirati Therapeutics, Inc., a Bristol Myers Squibb company. KRAZATI is a registered trademark of Mirati Therapeutics, Inc., a Bristol Myers Squibb company.

ABOUT KRAZATI (adagrasib)

KRAZATI (adagrasib) is highly selective and potent oral small-molecule inhibitor of KRASG12C that is optimized to sustain target inhibition, an attribute that could be important to treat KRASG12C-mutated cancers, as the KRASG12C protein regenerates every 24-48 hours. KRASG12C mutations act as oncogenic drivers and occur in approximately 14% of NSCLC (adenocarcinoma), 3-4% of colorectal cancers, and 1-2% of several other cancers.

In 2022, KRAZATI was granted accelerated approval for treatment of adult patients with KRASG12C-mutated locally advanced or metastatic non-small cell lung cancer (NSCLC), as determined by an FDA-approved test, who have received at least one prior systemic therapy. This indication is approved under accelerated approval based on objective response rate (ORR) and duration of response (DOR). Continued approval for this indication may be contingent upon verification and description of a clinical benefit in a confirmatory trial(s). In 2024, the European Commission (EC) granted conditional marketing authorization for KRAZATI as a targeted treatment option for adult patients with KRASG12C-mutated advanced NSCLC and disease progression after at least one prior systemic therapy.

KRAZATI continues to be evaluated as monotherapy and in combination with other anti-cancer therapies in patients with advanced KRASG12C-mutated solid tumors, including NSCLC and colorectal cancer.

In 2022, the FDA granted breakthrough therapy designation for KRAZATI in combination with cetuximab in patients with KRASG12C-mutated advanced colorectal cancer (CRC) whose cancer has progressed following prior treatment with chemotherapy and an anti-VEGF therapy.

For Prescribing Information, visit View Source

ABOUT KRYSTAL-1

KRYSTAL-1 is an open-label, multicenter, multiple expansion cohort Phase 1/2 trial to determine the safety and efficacy of KRAZATI in patients with advanced solid tumors that harbor a KRASG12C mutation. The primary endpoint for the Phase 2 cohort of the KRYSTAL-1 study was objective response rate. Secondary endpoints included duration of response, progression-free survival, overall survival and safety.

INDICATION

KRAZATI is indicated for the treatment of adult patients with KRASG12C-mutated locally advanced or metastatic non-small cell lung cancer (NSCLC), as determined by an FDA-approved test, who have received at least one prior systemic therapy.

This indication is approved under accelerated approval based on objective response rate (ORR) and duration of response (DOR). Continued approval for this indication may be contingent upon verification and description of a clinical benefit in a confirmatory trial(s).

IMPORTANT SAFETY INFORMATION

GASTROINTESTINAL ADVERSE REACTIONS

In the pooled safety population, serious gastrointestinal adverse reactions observed were gastrointestinal obstruction in 1.6%, including 1.4% grade 3 or 4, gastrointestinal bleeding in 0.5% of patients, including 0.5% grade 3, and colitis in 0.3%, including 0.3% grade 3. In addition, nausea, diarrhea, or vomiting occurred in 89% of 366 patients, including 9% grade 3. Nausea, diarrhea, or vomiting led to dosage interruption or dose reduction in 29% of patients and permanent discontinuation of KRAZATI in 0.3%
Monitor and manage patients using supportive care, including antidiarrheals, antiemetics, or fluid replacement, as indicated. Withhold, reduce the dose, or permanently discontinue KRAZATI based on severity
QTC INTERVAL PROLONGATION

KRAZATI can cause QTc interval prolongation, which can increase the risk for ventricular tachyarrhythmias (e.g., torsades de pointes) or sudden death
In the pooled safety population, 6% of 366 patients with at least one post-baseline electrocardiogram (ECG) assessment had an average QTc ≥501 ms, and 11% of patients had an increase from baseline of QTc >60 msec. KRAZATI causes concentration-dependent increases in the QTc interval
Avoid concomitant use of KRAZATI with other products with a known potential to prolong the QTc interval. Avoid use of KRAZATI in patients with congenital long QT syndrome and in patients with concurrent QTc prolongation
Monitor ECGs and electrolytes prior to starting KRAZATI, during concomitant use, and as clinically indicated in patients with congestive heart failure, bradyarrhythmias, electrolyte abnormalities, and in patients who are taking medications that are known to prolong the QT interval. Withhold, reduce the dose, or permanently discontinue KRAZATI, depending on severity
HEPATOTOXICITY

KRAZATI can cause hepatotoxicity
In the pooled safety population, hepatotoxicity occurred in 37%, and 7% were grade 3 or 4. A total of 32% of patients who received KRAZATI had increased alanine aminotransferase (ALT)/increased aspartate aminotransferase (AST); 5% were grade 3 and 0.5% were grade 4. Increased ALT/AST leading to dose interruption or reduction occurred in 11% of patients. KRAZATI was discontinued due to increased ALT/AST in 0.5% of patients
Monitor liver laboratory tests (AST, ALT, alkaline phosphatase, and total bilirubin) prior to the start of KRAZATI, and monthly for 3 months or as clinically indicated, with more frequent testing in patients who develop transaminase elevations. Reduce the dose, withhold, or permanently discontinue KRAZATI based on severity
INTERSTITIAL LUNG DISEASE /PNEUMONITIS

KRAZATI can cause interstitial lung disease (ILD)/pneumonitis, which can be fatal. In the pooled safety population, ILD/pneumonitis occurred in 4.1% of patients, 1.4% were grade 3 or 4, and 1 case was fatal. The median time to first onset for ILD/pneumonitis was 12 weeks (range: 5 to 31 weeks). KRAZATI was discontinued due to ILD/pneumonitis in 0.8% of patients
Monitor patients for new or worsening respiratory symptoms indicative of ILD/pneumonitis (eg, dyspnea, cough, fever). Withhold KRAZATI in patients with suspected ILD/pneumonitis and permanently discontinue KRAZATI if no other potential causes of ILD/pneumonitis are identified
ADVERSE REACTIONS

The most common adverse reactions (≥25%) are nausea, diarrhea, vomiting, fatigue, musculoskeletal pain, hepatotoxicity, renal impairment, edema, dyspnea, decreased appetite
FEMALES AND MALES OF REPRODUCTIVE POTENTIAL

Infertility: Based on findings from animal studies, KRAZATI may impair fertility in females and males of reproductive potential
Please see U.S. Full Prescribing Information for KRAZATI at View Source

About Colorectal Cancer

Colorectal cancer (CRC) is cancer that develops in the colon or the rectum, which are part of the body’s digestive or gastrointestinal system. CRC is the third most commonly diagnosed cancer in the world. In 2020, it is estimated that there were approximately 1,931,000 new cases of the disease; it is the second leading cause of cancer-related deaths among men and women combined.

Alligator Bioscience Announces Two Presentations on Mitazalimab and ATOR-4066 at the AACR Annual Meeting 2024

On April 8, 2024 Alligator Bioscience (Nasdaq Stockholm: ATORX) reported the company will give two presentations, one on mitazalimab, a CD40 agonist, and one on ATOR-4066, a Neo-X-Prime bispecific antibody (bsAb), at the Americal Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, taking place April 5-10, 2024, in San Diego, California (Press release, Alligator Bioscience, APR 8, 2024, View Source [SID1234641855]).

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

The first presentation, entitled "Mitazalimab, a potent CD40 agonist in combination with FOLFIRINOX demonstrates changes consistent with increased immune activation in TME and peripheral blood in a preclinical pancreatic cancer tumor model", provides further support to the unique dosing regimen chosen for the OPTIMIZE-1 Phase 2 study in first line metastatic pancreatic cancer, resulting in an increased tumoricidal immune profile, including a marked increase in effector CD8+ T cells in the tumor microenvironment. Taken together, these preclinical data provides a mechanistic explanation to the unprecedented DoR and OS observed in OPTIMIZE-1 and corroborates the previously reported associations between clinical response and T cell activation, highlighting the mitazalimab-specific contribution to tumor responses. Moreover, the presentation underlines the synergistic potential of this combination for an improved antitumor response compared to FOLFIRINOX alone.

The second presentation, entitled "ATOR-4066, a Neo-X-Prime bispecific antibody targeting CD40 and CEACAM5, induces tumor localized immune cell activation in preclinical in vivo tumor model", demonstrates that ATOR-4066 activates tumor infiltrating dendritic cells and macrophages resulting in increases in activated tumor infiltrating T cells, thus creating a pro-inflammatory tumor microenvironment leading to single-agent complete responses in translational tumor models. These data strongly support further development and clinical testing of ATOR-4066.

"We are very pleased to be presenting data for two of our promising CD40-candidates at this year’s prestigious AACR (Free AACR Whitepaper) Annual Meeting, which highlight the increasing strength and progress of our CD40 program," said Søren Bregenholt, CEO of Alligator Bioscience. "The first presentation details further supporting evidence of the potential of our lead asset mitazalimab to provide significant clinical benefit to pancreatic cancer patients in combination with chemotherapy when compared to standard of care, as demonstrated in the outstanding top-line results from our OPTIMIZE-1 study. The second presentation suggests CD40 could be activated in a very selective manner, which would open the way to an even more targeted therapeutic approach. These data strongly support the further development of ATOR-4066 in clincial trials, which Alligator is currently working toward."
Poster Presentation Details
Abstract Number: 2376
Title: Mitazalimab, a potent CD40 agonist in combination with FOLFIRINOX demonstrates changes consistent with increased immune activation in TME and peripheral blood in a preclinical pancreatic cancer tumor model
Date/Time: April 8, 2024, 9:00 AM – 12:30 PM PT
Session: PO.CL06.07 – Antibodies 1
Presenter: D. Gomez Jimenez, Translational Scientist, Alligator Bioscience
Location: Poster Section 38, Poster Board 22

Abstract Number: 5309
Title: ATOR-4066, a Neo-X-Prime bispecific antibody targeting CD40 and CEACAM5, induces tumor localized immune cell activation in preclinical in vivo tumor model
Date/Time: April 9, 2024, 1:30 PM – 5:00 PM PT
Session: PO.IM01.17 – Immune Modulation Employing Agonist or Co-Stimulatory Approaches
Presenter: Hampus Andersson, PhD Student, Alligator Bioscience
Location: Poster Section 3, Poster Board 18

Kineta Reports Initial Clinical Response Data at AACR 2024 of its Ongoing Phase 1/2 VISTA-101 Clinical Trial

On April 8, 2024 Kineta, Inc. (Nasdaq: KA), a clinical-stage biotechnology company focused on the development of novel immunotherapies in oncology that address cancer immune resistance, reported at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) in San Diego, CA an update on its ongoing VISTA-101 Phase 1/2 clinical trial evaluating KVA12123, an anti-VISTA monoclonal antibody, as monotherapy and in combination with Merck’s anti-PD1 therapy, KEYTRUDA (pembrolizumab), in patients with advanced solid tumors (Press release, Kineta, APR 8, 2024, View Source [SID1234641854]).

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

KVA12123 cleared the fifth of six monotherapy dose levels and the second of four cohorts in combination with pembrolizumab. KVA12123 was well tolerated with no dose limiting toxicities (DLT) or cytokine related adverse events at any dose level.

The poster presentation #CT068: "Interim results of the ongoing phase 1/2 clinical trial of KVA12123, an engineered IgG1 targeting VISTA, alone and in combination with pembrolizumab in advanced solid tumors" was presented Monday, April 8, 2024 and reported the following findings (the data cutoff date was February 28, 2024):

Monotherapy Dose Escalation (3 – 300 mg KVA12123 Q2W)


Of 21 patients enrolled, 12 received at least one baseline and one follow up scan

Best overall response (BOR) in 9 of 12 patients with at least one follow-up scan is stable disease with a mean duration of 15 weeks

One patient with non-small cell lung cancer that failed 6 prior lines of therapy, including checkpoint inhibitor (CPI) therapy, has experienced stable disease lasting 28 weeks

Nine participants remain on-treatment

Combination Therapy Dose Escalation (30-100 mg KVA12123 Q2W, 400 mg pembrolizumab Q6W) Of 9 patients enrolled, 3 received at least one baseline and one follow-up scan

BOR in 2 of 3 patients with at least one follow up scan is:
o
Partial Response in 1 mucoepidermoid carcinoma patient with a 54% reduction in target lesions and a complete response in non-target lesions
o
Stable disease in 1 renal cell carcinoma patient that had progressed on prior CPI therapy with a 24% reduction in target lesions

Eight patients remain on-treatment

Biomarkers


Dose-dependent induction of on-target pro-inflammatory cytokines and chemokines

Dose-dependent increases in activated non-classical monocytes, CD4+ and CD8+ T cells, and NK cells

Safety


No DLTs observed in any patient at any dose level

No evidence of cytokine release syndrome in any patient at any dose level

"We are pleased to present our progress on the VISTA-101 clinical trial at AACR (Free AACR Whitepaper) this year, with the initial clinical response data and the durability of patient benefit emerging from the study. The safety profile of KVA12123 to date has been remarkable in the monotherapy as well as combotherapy cohorts, supporting advancement to the final monotherapy dosing cohort of KVA12123 and reaching the estimated optimal therapeutic dose," said Thierry Guillaudeux, Ph.D., Chief Scientific Officer of Kineta. "Initial read-outs demonstrated that KVA12123 is not only safe but exhibits potential clinical benefit for some patients as either monotherapy or combotherapy and may offer patients a novel approach to address immunosuppression in the tumor microenvironment and better manage solid tumor cancers." In February 2024, the company announced that it is pursuing strategic alternatives to maximize shareholder value due to certain investors indicating they will not fulfill their April 2024 funding obligation in the previously disclosed private placement financing. As a result, the company has suspended new patient enrollment into the Phase 1/2 VISTA-101 trial and will not be recruiting patients into either the sixth cohort in the monotherapy arm or the third cohort in the combination therapy arm. Patients currently enrolled in the trial will be permitted to continue to participate.

KEYTRUDA is a registered trademark of Merck Sharp & Dohme LLC, a subsidiary of Merck & Co., Inc., Rahway, NJ, USA.

Medicxi and Starpharma create Petalion Therapeutics to develop novel dendrimer-based treatments

On April 8, 2024 Starpharma reported it has entered into a strategic partnership with Medicxi, a leading life sciences investment firm dedicated to financing companies developing innovative medicines, to co-found a new UK-based company called Petalion Therapeutics Limited ("Petalion") (Press release, Starpharma, APR 8, 2024, View Source;mc_eid=bf52dd3418 [SID1234641853]).

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

Petalion will initially focus on developing novel targeted dendrimer-drug conjugate therapies in oncology, utilising Starpharma’s proprietary DEP dendrimer platform technology.

Medicxi will fund Petalion with an initial investment of up to USD $25 million (~AUD $38 million) to finance the development of a novel oncology drug candidate. Starpharma will license certain intellectual property ("IP") to Petalion as required for the research, development, manufacture and commercialisation of this potential new therapeutic and, in exchange, will receive an equity holding of 22.5% in Petalion.

Collaboration Agreement

Under the terms of the collaboration, Starpharma will license the IP to Petalion on an exclusive basis for a mutually agreed target. In consideration for the IP licence to this specific target, Starpharma will be issued ordinary shares in Petalion. Starpharma will also provide R&D services to Petalion on a fee for service basis.

Medicxi intends to finance Petalion’s development program via a tranched investment plan with defined scientific and technical milestones, culminating in a total investment of up to USD $25 million.

Dr Mehdi Shahidi, a highly experienced pharmaceutical executive, has been appointed as CEO of Petalion. A clinical oncologist by background, Dr Shahidi has over two decades of experience in pharmaceutical drug development, most recently as Corporate Senior Vice President, Chief Medical Officer, and Global Head of Medicine at Boehringer Ingelheim.

Dr Mehdi Shahidi, CEO of Petalion and Venture Partner at Medicxi, commented:

"I am deeply honoured and thrilled to be leading this ground-breaking endeavour created by Medicxi and Starpharma. Leveraging Starpharma’s world-leading technology and the scientific domain expertise from Medicxi’s asset-centric investment platform, our team at Petalion aims to develop best-in-class dendrimer conjugates with differentiated properties. Our ultimate goal is to cultivate a targeted dendrimer-based drug that can effectively address unmet needs in cancer."

Shyam Masrani, Principal at Medicxi and Board representative of Petalion, commented:

"While the field of targeted conjugates has experienced remarkable growth and led to the approval of several treatment options for patients with cancer, it is also evident that the current approaches have limitations. Medicxi is excited to support Petalion under the leadership of Dr Shahidi from the outset and we look forward to working closely with the Starpharma team to develop a highly differentiated and effective new medicine."

Cheryl Maley, CEO of Starpharma, commented:

"We are excited to announce this strategic partnership, which combines Starpharma’s expertise in developing dendrimer technology with Medicxi’s success in converting development candidates into high-value commercial assets. If successful, the oncology therapies that Petalion will develop have the potential to become an important treatment modality for a potentially wide range of cancer indications.

"Medicxi is a highly innovative organisation with extensive experience in drug development and commercialisation. Their investment in this partnership validates the strong potential of Starpharma’s DEP dendrimer technology as a novel drug delivery platform.

"This is just one of many ongoing efforts to prioritise the commercialisation of Starpharma’s DEP platform and our partnerships to advance the application of the DEP technology in high-value novel therapeutic areas."