The Role of YAP1 in Fibrosis Explored Through Its Local Inhibition With Verteporfin in Surgical Wounds: A Randomized Controlled, Prospective, Evaluator-blinded Proof-of-concept Study.

When we get injured, our body naturally tries to heal. In adults, this healing often leads to scars - thick, stiff tissue known as fibrotic tissue. Unlike normal tissue, fibrotic tissue doesn't function properly and can cause serious health problems, depending on the affected organ. Once it forms, fibrosis is usually permanent.
A good example of the fibrosis process is the healing of our skin: after a cut or surgery, the resulting scar is a type of fibrosis. Special cells called fibroblasts are key players in this process.
Our study looks at a drug called verteporfin, which is already approved both in Europe and the U.S. Previous research on mice and human cells suggests it can reduce or even prevent fibrosis.
We are now testing, clinically, histologically and by scRNA-seq, whether injecting verteporfin into the skin during wound healing, specifically after surgical procedures, can prevent thick, rigid scars from forming. Since the skin is easy to observe and sample, it offers a great model for studying this.
Will verteporfin have an impact on how surgical wounds heal? That's what we aim to find out.

Start Date08 May 2025

Sponsor / Collaborator

Les Hôpitaux Universitaires de Genève

[+2]

NCT06807359

/ RecruitingPhase 1/2

Open-label Clinical Phase 1/2 Study to Assess the Safety and Efficacy of the SpectraCure P18 System and Verteporfin for Injection for the Treatment of Primary Localized Prostate Cancer

The goal of this study is to obtain safety data, establish dose parameters, and effectiveness of treatment for the SpectraCure P18 System with IDOSE®, together with verteporfin for injection (VFI) as photosensitizer, for the treatment of primary localized prostate cancer.
The study will be divided into two parts, with Phase I, dose-escalation, to study safety and establish an effective light dose, followed by Phase II, cohort expansion, to evaluate clinical efficacy and confirm safety/tolerability. The subjects will be followed for a period of 18 months to determine the primary outcome. The long-term follow-up is an additional 18 months, i.e. a total of 36 months.
Interstitial Photodynamic Therapy (PDT) will be performed during general anesthesia. Optical fibers will be inserted into the prostate with a transperineal approach using transrectal ultrasound guidance. The intent is to deliver an adequate light dose throughout the prostate. Subjects will receive VFI intravenously, approximately 60-90 minutes prior to light delivery.

Start Date06 Jan 2025

Sponsor / Collaborator

SpectraCure AB

NCT06381154

/ RecruitingPhase 2IIT

Photodynamic Priming to Facilitate Immunologic Activity of Anti-PD1 in Patients With Pancreatic Cancer

This phase II trial tests how well photoradiation with verteporfin and pembrolizumab plus standard of care chemotherapy works in treating patients with pancreatic cancer that cannot be removed by surgery (unresectable), that has spread to nearby tissue or lymph nodes (locally advanced) or to other places in the body (metastatic). Photoradiation uses light activated drugs, such as verteporfin, that become active when exposed to light. These activated drugs may kill tumor cells. Vertoporfin may also increase tumor response to immunotherapy. Immunotherapy with monoclonal antibodies, such as pembrolizumab, may help the body's immune system attack the cancer, and may interfere with the ability of tumor cells to grow and spread. Chemotherapy drugs, such as modified fluorouracil, leucovorin, irinotecan, and oxaliplatin (mFOLFIRINOX), work in different ways to stop the growth of tumor cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Photoradiation with verteporfin and pembrolizumab plus standard of care chemotherapy may kill more tumor cells in patients with unresectable, locally advanced or metastatic pancreatic cancer.

Start Date06 Dec 2024

Sponsor / Collaborator

Mayo Clinic

[+1]

100 Clinical Results associated with Verteporfin

100 Translational Medicine associated with Verteporfin

100 Patents (Medical) associated with Verteporfin

1,868

Literatures (Medical) associated with Verteporfin

01 Feb 2026·TISSUE & CELL

Lysophosphatidic acid-induced YAP activation regulates osteogenesis of MC3T3-E1

Article

Author: Gong, Ping ; Zhang, Qin ; Xiang, Lin ; Yuan, Ying ; Wu, Bingfeng ; Liu, Jiayi

Lysophosphatidic acid (LPA) is a small bioactive lysophospholipid that elicits diverse biological activities in bone homeostasis and diseases. However, the specific functions of LPA and intrinsic mechanism underlying these processes is not well understood. In this study, we identified that LPA regulated cell proliferation, migration, and osteogenic differentiation primarily via LPA₁ in MC3T3-E1 pre-osteoblastic cells. More importantly, western blot analysis indicated that LPA stimulated the activation of the transcriptional regulator YAP via the Hippo pathway kinases LATS, but had negligible effects on MST. Moreover, verteporfin was applied to block YAP, which further elucidated the effects of LPA-induced YAP activation on osteogenesis. Interestingly, Rho-kinase (ROCK) might also be involved in LPA-induced YAP nuclear localization and dephosphorylation. Taken together, these data provide novel insights into the molecular mechanisms of LPA in bone homeostasis and regeneration.

01 Jan 2026·TOXICOLOGY

Microplastics and nanoplastics, emerging pollutants, increased the risk of pulmonary fibrosis in vivo and in vitro: A comparative evaluation of their potential toxicity effects with different polymers and size

Article

Author: Wang, Chen-Yu ; Wu, Yan-Ling ; Dou, Jia-Yi ; Dai, Xu ; Liu, Sen ; Lian, Li-Hua ; Nan, Ji-Xing ; Cui, Zhen-Yu

With the increasing consumption of plastic products, microplastics (MPs) and nanoplastics (NPs), as new environmental pollution, pose a huge potential threat to human health. The different polymers and sizes of MPs and NPs are important factors determining the distribution and pathways of particulate organisms, thereby affecting their toxicity. The study explored the pulmonary toxicity and potential mechanism of MPs (1 μm) and NPs (100nm) of polystyrene (PS), polyethylene (PE), or polypropylene (PP) in vivo and in vitro. Intratracheal injection of MPs/NPs (10mg/kg, once every six days, continued four times) in mice induced pulmonary histopathological changes, raised α-SMA and collagen I expressions, the TIMP-1/MMP13 ratio, epithelial-mesenchymal transition (EMT)-related proteins, recruited immune cells and increased pro-inflammatory cytokine secretion, especially in PS-NPs group. MPs/NPs (PS, PE or PP) exhibited cytotoxicity in human lung epithelial BEAS-2B, and MPs/NPs (50μg/mL, 8h) up-regulated α-SMA, Vimentin, and IL-1β expressions. PS-NPs raised YAP1 and inhibited FXR expression in mice or BEAS-2B, compared with other polymers or diameters. In PS-NPs-induced BEAS-2B, Verteporfin (YAP1 antagonist, 0.2μM) or GW4064 (FXR agonist, 2μM) reduced α-SMA, Vimentin, and IL-1β expressions, while Gugglesterone (FXR antagonist, 50μM) increased above protein expressions. Meanwhile, FXR deficiency increased YAP1 activity and fibrogenesis in PS-NPs-induced BEAS-2B. Collectively, MPs/NPs exposure elevates the risk of pulmonary fibrosis, and FXR-YAP1 axis dysregulation may underlie their toxicity mechanisms. Among the tested polymers, PS exhibits stronger pulmonary toxicity and cytotoxicity compared to PE or PP, and NPs of the same polymer demonstrate greater pulmonary toxicity than MPs.

01 Dec 2025·MOLECULAR BIOLOGY REPORTS

Targeting breast cancer stem cells in ER-positive breast cancer by repurposing the benzoporphyrin derivative verteporfin as a YAP/TAZ small molecule inhibitor

Article

Author: Roy, Himansu ; Chatterji, Urmi ; Talukdar, Priyanka Dey

BACKGROUND:

Current treatment strategies for hormone-dependent breast cancers, including adjuvant endocrine therapy, often fail due to persistence of breast cancer stem cells (brCSCs), which are significant contributors to tumor recurrence and treatment resistance. Therefore, gaining deeper insights into the molecular regulators driving breast cancer aggressiveness is important. Moreover, given the complexities and expenses involved in developing new pharmacological agents, the strategic repurposing of existing FDA-approved drugs to target these key molecular pathways presents a compelling approach for identifying novel therapeutic interventions aimed at mitigating tumor refractoriness.

METHODS:

The study employs survival analysis from TCGA database, protein expression analyses alongside aldefluor assays, sphere formation efficiency tests to evaluate cellular stemness, and DCFDA analysis combined with antioxidant enzyme assays to investigate redox imbalance in brCSCs. These analyses were conducted following the genetic deletion of YAP/TAZ and pharmacological treatment with verteporfin.

RESULTS:

The study demonstrated that transcriptional co-activators YAP/TAZ are significantly upregulated in chemotreated ER⁺ patient breast tumors and MCF-7 mammospheres, where it was found to interact with the transcription factor SOX2 within the nuclear compartment. Genetic ablation and pharmacological inhibition of YAP/TAZ markedly impaired stemness properties and disrupted redox homeostasis in the mammospheres. Additionally, treatment with verteporfin led to a substantial reduction in the frequency and viability of brCSCs, suggesting their effective eradication.

CONCLUSION:

This study highlights the potential of repurposing verteporfin, an FDA-approved drug originally formulated for age-related macular degeneration, as a therapeutic agent for targeting YAP/TAZ-mediated stemness and redox balance in brCSCs, thereby reducing their viability in ER-positive breast cancers.

News (Medical) associated with Verteporfin

01 Nov 2023

·www.globenewswire.com

Research Funded by Bay Area Lyme Foundation Identifies New Investigational Therapy Regimen Capable of Irreversibly Damaging Lyme Bacteria in Laboratory Tests

Inspired by research that targets cancer tumors, these new findings in Lyme could also lead to novel R&D strategies for other diseasesPORTOLA VALLEY, Calif., Nov. 01, 2023 (GLOBE NEWSWIRE) -- Bay Area Lyme Foundation, a leading sponsor of Lyme disease research in the US, today announced the development of a potential new drug, HS-291, that targets and destroys Borrelia burgdorferi, the bacterium that causes Lyme disease. Published in the peer-reviewed journal Cell Chemical Biology, this laboratory study represents a novel paradigm shift for anti-microbial treatment research as it is the first to target and inhibit Borrelia burgdorferi HtpG (high temperature protein G), a specific type of enzyme within the bacteria that causes Lyme disease— a condition affecting nearly 500,000 new patients annually. The research was conducted at Duke University School of Medicine, with collaboration from University of North Carolina, Tulane University, and Stanford University, and HS-291 is currently in preclinical stage testing at UC Davis. “As Lyme disease is currently treated with broad spectrum antibiotics and there are no targeted treatments, we are particularly excited about this discovery, and hopeful that our novel Lyme disease therapeutic HS-291 will specifically destroy the Lyme bacterium without off-target effects or antibiotic resistance,” said Timothy Haystead, PhD, professor of Pharmacology and Cancer Biology, Duke University School of Medicine, Bay Area Lyme Foundation grantee, and co-lead author. “This research has been an incredible opportunity to leverage knowledge from oncology to Lyme disease in order to design an investigational therapeutic that could one day benefit hundreds of thousands of patients with Lyme.” This new discovery has implications beyond Lyme disease as it demonstrates that using the drug HS-291 to deliver cellular toxins to HtpG, a type of non-essential enzyme that assists the folding or unfolding of large and complex proteins, greatly expands what can be considered druggable within any pathogen and opens a whole new area of infectious disease research. When activated, HS-291, an inhibitor of HtpG tethered to the photoactive cellular toxin verteporfin, causes discrete protein modifications, which wreaks havoc on the Lyme disease bacterium’s DNA. This impacts multiple processes including nucleoid collapse and cell wall disruptions. A single dose of HS-291, when activated by light, irreversibly damages Borrelia proteins in close proximity of Bb HtpG in vitro. “Antibiotics used to treat Lyme disease do not always work for all patients, which causes many to suffer for years with extreme symptoms including neurocognitive issues, disabling fatigue and sleep disruption,” said Linda Giampa, executive director of the Bay Area Lyme Foundation. “Bay Area Lyme concentrates on funding innovative research, including projects where knowledge can be deployed from other areas of medicine. We hope that this discovery will inspire others to join us in investing in impactful, translational research to bring relief to patients.” This research was made possible by a 2020 Bay Area Lyme Foundation grant of more than $2 million to Duke University School of Medicine in honor of Neil Spector, MD, a renowned oncologist who passed away from complications of Lyme disease that had been misdiagnosed for years. He encouraged scientists to take cancer staging techniques and immunotherapy learnings from oncology and apply them to Lyme research. Dr. Spector was the Sandra Coates associate professor in the Duke University Department of Medicine and also served on Bay Area Lyme Foundation’s Scientific Advisory Board. Haystead and Spector joined forces as Spector sought to leverage his knowledge of oncology to help better understand Lyme disease, and Haystead’s research is focused on the use of chemical biology approaches to define novel drug targets focused on the treatment of hypertension, obesity, cancer, inflammatory and infectious disease. Bay Area Lyme Foundation also funded University of North Carolina collaborator, Matt Redinbo, PhD’s research on HS-291; his lab’s crystallography work was instrumental in the discovery process. Bay Area Lyme Foundation’s research grant program was made possible by the support from the Fairbairn Family, the Younger Family Fund, and Project Lyme. About Lyme disease The most common vector-borne infectious disease in the US, Lyme disease is a potentially disabling infection caused by bacteria transmitted through the bite of an infected tick to people and pets, and may also be passed from a pregnant mother to her unborn baby. If caught early, most cases of Lyme disease can be effectively treated, but it is commonly misdiagnosed due to lack of awareness and inaccurate diagnostic tests. There are approximately 500,000 new cases of Lyme disease each year, according to statistics released in 2018 by the CDC. As a result of the difficulty in diagnosing and treating Lyme disease, up to two million Americans may be suffering from the impact of its debilitating long-term symptoms and complications, according to Bay Area Lyme Foundation estimates. About Bay Area Lyme Foundation Bay Area Lyme Foundation, a national organization committed to making Lyme disease easy to diagnose and simple to cure, is the leading public not-for-profit sponsor of innovative Lyme disease research in the US. A 501c3 organization based in Silicon Valley, Bay Area Lyme Foundation collaborates with world-class scientists and institutions to accelerate medical breakthroughs for Lyme disease. It is also dedicated to providing reliable, fact-based information so that prevention and the importance of early treatment are common knowledge. A pivotal donation from The LaureL STEM FUND covers overhead costs and allows for 100% of all donor contributions to the Bay Area Lyme Foundation to go directly to research and prevention programs. For more information about Lyme disease or to get involved, visit www.bayarealyme.org or call us at 650-530-2439. Media contact:Tara DiMiliaPhone: 908-369-7168Tara.DiMilia@tmstrat.com

04 Oct 2023

·www.biospace.com

CIMERLI® (ranibizumab-eqrn) Sales Exceed 100,000 Doses in First Year of Launch

CIMERLI® is the #1 ranibizumab biosimilar with 25% ranibizumab market share* Demonstrated safety and efficacy in clinical trials and real-world settings Robust and reliable supply addresses market need and expands anti-VEGF options across the retinal market REDWOOD CITY, Calif., Oct. 04, 2023 (GLOBE NEWSWIRE) -- Coherus BioSciences, Inc. (Coherus, Nasdaq: CHRS), today announced that sales of CIMERLI® (ranibizumab-eqrn) to retinal specialists have exceeded 100,000 doses since commercial launch on October 3, 2022. CIMERLI® is the first and only FDA-approved biosimilar interchangeable with Lucentis® for all approved indications. In August 2023, CIMERLI® achieved 25% market share of the ranibizumab market*, making it the #1 ranibizumab biosimilar. “Eclipsing 100,000 doses sold to retinal specialists within the first full year after commercial launch is an important milestone for CIMERLI® and reinforces the retinal community’s desire for a safe and effective biosimilar option to LUCENTIS®,” said Paul Reider, Chief Commercial Officer of Coherus. “Achieving 25% market share speaks to the strength of our commercial capabilities and replicates the success we saw with UDENYCA® in its first year on the market. We look forward to potential continued sales growth for CIMERLI® as more accounts continue their conversion.” “Over the past twelve months we have launched three new products: CIMERLI®, the UDENYCA® auto-injector and YUSIMRY™. We now look forward to the potential approvals of two more products this year: toripalimab for nasopharyngeal carcinoma and the UDENYCA® on-body injector, and their subsequent launches,” said Denny Lanfear, Chairman and Chief Executive Officer of Coherus. Coherus plans to report CIMERLI® net sales for the third quarter when the company reports Q3 2023 financial results in November. About CIMERLI® CIMERLI® (ranibizumab-eqrn) is the only FDA-approved biosimilar interchangeable with Lucentis® for all Lucentis® FDA-approved indications. Formerly CHS-201 (also known as FYB201), it is a biosimilar to the reference product, U.S.-licensed Lucentis®. CIMERLI® has the same product attributes as Lucentis®, in terms of dosage strengths (0.3 mg, 0.5 mg), formulation and excipients, and amino acid sequence. CIMERLI® was approved by the FDA on August 2, 2022. Coherus owns the biologics license application (BLA) for CIMERLI® and commercial rights in the U.S. and its territories. Coherus licensed CIMERLI® from Bioeq AG, a joint venture between Polpharma Biologics Group B.V. and Formycon AG. *IQVIA NSP Data August 2023. 1. CIMERLI® (ranibizumab-eqrn) U.S. Prescribing Information, August 2022. IMPORTANT SAFETY INFORMATION & INDICATIONS CIMERLI® (ranibizumab-eqrn) is interchangeable* to Lucentis® (ranibizumab injection) CIMERLI® (ranibizumab-eqrn), a vascular endothelial growth factor (VEGF) inhibitor, is indicated for the treatment of patients with: Neovascular (Wet) Age-Related Macular Degeneration (AMD) Macular Edema Following Retinal Vein Occlusion (RVO) Diabetic Macular Edema (DME) Diabetic Retinopathy (DR) Myopic Choroidal Neovascularization (mCNV) CONTRAINDICATIONS CIMERLI® is contraindicated in patients with ocular or periocular infections or known hypersensitivity to ranibizumab products or any of the excipients in CIMERLI®. Hypersensitivity reactions may manifest as severe intraocular inflammation WARNINGS AND PRECAUTIONS Endophthalmitis and Retinal Detachments: Intravitreal injections, including those with ranibizumab products, have been associated with endophthalmitis and retinal detachments. Proper aseptic injection technique should always be utilized when administering CIMERLI®. Patients should be monitored following the injection to permit early treatment, should an infection occur Increases in Intraocular Pressure: Increases in intraocular pressure (IOP) have been noted both pre-injection and post-injection (at 60 minutes) with ranibizumab products. Monitor intraocular pressure prior to and following intravitreal injection with CIMERLI® and manage appropriately Thromboembolic Events: Although there was a low rate of arterial thromboembolic events (ATEs) observed in the ranibizumab clinical trials, there is a potential risk of ATEs following intravitreal use of VEGF inhibitors. ATEs are defined as nonfatal stroke, nonfatal myocardial infarction, or vascular death (including deaths of unknown cause) Neovascular (wet) age-related macular degeneration The ATE rate in the 3 controlled neovascular AMD studies during the first year was 1.9% (17 of 874) in the combined group of patients treated with 0.3 mg or 0.5 mg ranibizumab compared with 1.1% (5 of 441) in patients from the control arms. In the second year of Studies AMD-1 and AMD-2, the ATE rate was 2.6% (19 of 721) in the combined group of ranibizumab-treated patients compared with 2.9% (10 of 344) in patients from the control arms. In Study AMD-4, the ATE rates observed in the 0.5 mg arms during the first and second year were similar to rates observed in Studies AMD-1, AMD-2, and AMD-3 In a pooled analysis of 2-year controlled studies (AMD-1, AMD-2, and a study of ranibizumab used adjunctively with verteporfin photodynamic therapy), the stroke rate (including both ischemic and hemorrhagic stroke) was 2.7% (13 of 484) in patients treated with 0.5 mg ranibizumab compared to 1.1% (5 of 435) in patients in the control arms (odds ratio 2.2 [95% confidence interval (0.8-7.1)]) Macular edema following retinal vein occlusion The ATE rate in the 2 controlled RVO studies during the first 6 months was 0.8% in both the ranibizumab and control arms of the studies (4 of 525 in the combined group of patients treated with 0.3 mg or 0.5 mg ranibizumab and 2 of 260 in the control arms). The stroke rate was 0.2% (1 of 525) in the combined group of ranibizumab-treated patients compared to 0.4% (1 of 260) in the control arms Diabetic macular edema and Diabetic Retinopathy In a pooled analysis of Studies D-1 and D-2, the ATE rate at 2 years was 7.2% (18 of 250) with 0.5 mg ranibizumab, 5.6% (14 of 250) with 0.3 mg ranibizumab, and 5.2% (13 of 250) with control. The stroke rate at 2 years was 3.2% (8 of 250) with 0.5 mg ranibizumab, 1.2% (3 of 250) with 0.3 mg ranibizumab, and 1.6% (4 of 250) with control. At 3 years, the ATE rate was 10.4% (26 of 249) with 0.5 mg ranibizumab and 10.8% (27 of 250) with 0.3 mg ranibizumab; the stroke rate was 4.8% (12 of 249) with 0.5 mg ranibizumab and 2.0% (5 of 250) with 0.3 mg ranibizumab Fatal events in patients with diabetic macular edema and diabetic retinopathy at baseline: A pooled analysis of Studies D-1 and D-2 showed that fatalities in the first 2 years occurred in 4.4% (11 of 250) of patients treated with 0.5 mg ranibizumab, in 2.8% (7 of 250) of patients treated with 0.3 mg ranibizumab, and in 1.2% (3 of 250) of control patients. Over 3 years, fatalities occurred in 6.4% (16 of 249) of patients treated with 0.5 mg ranibizumab and in 4.4% (11 of 250) of patients treated with 0.3 mg ranibizumab. Although the rate of fatal events was low and included causes of death typical of patients with advanced diabetic complications, a potential relationship between these events and intravitreal use of VEGF inhibitors cannot be excluded ADVERSE REACTIONS Serious adverse events related to the injection procedure have occurred in <0.1% of intravitreal injections, including endophthalmitis, rhegmatogenous retinal detachment, and iatrogenic traumatic cataract In ranibizumab-treated patients compared with the control group, the most common ocular side effects included conjunctival hemorrhage, eye pain, vitreous floaters, and intraocular pressure. The most common non-ocular side effects included nasopharyngitis, anemia, nausea, and cough As with all therapeutic proteins, there is the potential for an immune response in patients treated with ranibizumab products. The clinical significance of immunoreactivity to ranibizumab products is unclear at this time Postmarketing Experience The following adverse reaction has been identified during post-approval use of ranibizumab products: Ocular: Tear of retinal pigment epithelium among patients with neovascular AMD *An interchangeable product (IP) is a biological product that is approved based on data demonstrating that it is highly similar to an FDA-approved reference product (RP) and that there are no clinically meaningful differences between the products; it can be expected to produce the same clinical result as the RP in any given patient; and if administered more than once to a patient, the risk in terms of safety or diminished efficacy from alternating or switching between use of the RP and IP is not greater than that from the RP without such alternation or switch. Interchangeability of CIMERLI® has been demonstrated for the condition(s) of use, strength(s), dosage form(s), and route(s) of administration described in its Full Prescribing Information To report SUSPECTED ADVERSE REACTIONS, contact Coherus BioSciences at 1-800-483-3692 or FDA at 1-800-FDA-1088 or . For additional Safety Information, please see CIMERLI® Full Prescribing Information available here. About Coherus BioSciences Coherus is a commercial-stage biopharmaceutical company focused on the research, development and commercialization of innovative immunotherapies to treat cancer. Coherus’ strategy is to build a leading immuno-oncology franchise funded with cash generated through net sales of its diversified portfolio of FDA-approved therapeutics. In 2021, Coherus in-licensed toripalimab, an anti-PD-1 antibody, in the United States and Canada. The Biologics License Application for toripalimab in combination with chemotherapy as treatment for recurrent or metastatic nasopharyngeal carcinoma is currently under review by the FDA. Coherus markets UDENYCA® (pegfilgrastim-cbqv), a biosimilar of Neulasta®, CIMERLI® (ranibizumab-eqrn), a biosimilar of Lucentis®, and YUSIMRY™ (adalimumab-aqvh), a biosimilar of Humira®. Forward-Looking Statements Except for the historical information contained herein, the matters set forth in this press release are forward-looking statements within the meaning of the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995, including, but not limited to, statements regarding Coherus’ ability to build its immuno-oncology franchise to achieve a leading market position; Coherus’ ability to generate cash and net sales; Coherus’ investment plans; Coherus’ ability to achieve approvals or launches of any of its product candidates; and expectations about maintaining or growing sales for any of Coherus’ products. Such forward-looking statements involve substantial risks and uncertainties that could cause Coherus’ actual results, performance or achievements to differ significantly from any future results, performance or achievements expressed or implied by the forward-looking statements. Such risks and uncertainties include, among others, the risks and uncertainties inherent in the clinical drug development process; risks related to integration of Surface Oncology, Inc.’s programs and operations; risks related to Coherus’ existing and potential collaboration partners; risks of Coherus’ competitive position; the risks and uncertainties of the regulatory approval process, including the speed of regulatory review, international aspects of Coherus’ business and the timing of Coherus’ regulatory filings; the risk of FDA review issues; the risk that Coherus is unable to complete commercial transactions and other matters that could affect the availability or commercial potential of Coherus’ products and product candidates; and the risks and uncertainties of possible litigation. All forward-looking statements contained in this press release speak only as of the date of this press release. Coherus undertakes no obligation to update or revise any forward-looking statements. For a further description of the significant risks and uncertainties that could cause actual results to differ from those expressed in these forward-looking statements, as well as risks relating to Coherus’ business in general, see Coherus’ Quarterly Report on Form 10-Q for the fiscal quarter ended June 30, 2023 filed with the Securities and Exchange Commission on August 2, 2023, including the section therein captioned “Risk Factors” and in other documents Coherus files with the Securities and Exchange Commission. UDENYCA®, CIMERLI® and YUSIMRY™, whether or not appearing in large print or with the trademark symbol, are trademarks of Coherus, its affiliates, related companies or its licensors or joint venture partners unless otherwise noted. Trademarks and trade names of other companies appearing in this press release are, to the knowledge of Coherus, the property of their respective owners. Coherus Contact Information: For Investors & Media Jodi Sievers, VP, Corporate Communications ir@coherus.com

Drug ApprovalClinical ResultBiosimilar

13 Feb 2023

·www.biospace.com

Coherus Granted Permanent, Product-Specific Q-Code for CIMERLI® (ranibizumab-eqrn) from the Centers for Medicare and Medicaid Services

- Q-Code assigned to CIMERLI® for Medicare claims processing effective for dates of service on and after April 1, 2023 - - COHERUS Solutions™ patient services hub is available to facilitate successful access and reimbursement - REDWOOD CITY, Calif., Feb. 13, 2023 (GLOBE NEWSWIRE) -- Coherus BioSciences Inc. (“Coherus”, Nasdaq: CHRS) today announced that the Centers for Medicare and Medicaid Services (CMS) has published a new code pursuant to the Company’s application for Healthcare Common Procedure Coding System (HCPCS) Q-codes. The HCPCS Q-code assigned to CIMERLI® will be effective for patients administered CIMERLI® on or after April 1, 2023. Paul Reider, Chief Commercial Officer of Coherus, said, "This is an important milestone in the CIMERLI® launch. Beginning April 1st, use of CIMERLI’s permanent, product-specific Q-code will enable more efficient billing processes and speed time to reimbursement for providers. We believe that Q-code utilization will serve as a catalyst for market conversion, accelerating growth in 2023 starting in the second quarter. We want to thank CMS for its consideration and timely review of our Q-code application.” CIMERLI® is the first and only FDA-approved biosimilar interchangeable with Lucentis® (ranibizumab injection) for all indications including neovascular (wet) age-related macular degeneration (AMD), macular edema following retinal vein occlusion (RVO), diabetic macular edema (DME), diabetic retinopathy (DR), and myopic choroidal neovascularization (mCNV). CIMERLI® is contraindicated in patients with ocular or periocular infections or known hypersensitivity to ranibizumab products or any of the excipients in CIMERLI®. Hypersensitivity reactions may manifest as severe intraocular inflammation.1 Coherus Solutions™ offers healthcare professionals comprehensive practice and patient support that includes extensive patient assistance, industry-leading electronic services, and office support to ensure successful access and reimbursement. About Q-Codes Q-codes are permanent reimbursement codes granted to biosimilars and used by commercial insurance plans, Medicare, Medicare Advantage, and other government payers for Medicare Part B drugs like CIMERLI® that are administered by a physician. Claims submission and documentation are simplified with a permanent Q-code, facilitating and streamlining the billing and reimbursement process. About CIMERLI® CIMERLI® (ranibizumab-eqrn) is the first and only FDA-approved biosimilar interchangeable with Lucentis® for all Lucentis® FDA-approved indications. CIMERLI® has the same product attributes with Lucentis®, in terms of dosage strengths (0.3 mg, 0.5 mg), formulation and excipients, and amino acid sequence. CIMERLI® was approved by the FDA on August 2, 2022. Coherus owns the biologics license application (BLA) and commercial rights in the U.S. and its territories. Coherus licensed CIMERLI® from Bioeq AG, a joint venture between Polpharma Biologics Group B.V. and Formycon AG. 1. CIMERLI® (ranibizumab-eqrn) U.S. Prescribing Information, August 2022. IMPORTANT SAFETY INFORMATION & INDICATIONS CIMERLI® (ranibizumab-eqrn) is interchangeable* to Lucentis® (ranibizumab injection) CIMERLI® (ranibizumab-eqrn), a vascular endothelial growth factor (VEGF) inhibitor, is indicated for the treatment of patients with: Neovascular (Wet) Age-Related Macular Degeneration (AMD) Macular Edema Following Retinal Vein Occlusion (RVO) Diabetic Macular Edema (DME) Diabetic Retinopathy (DR) Myopic Choroidal Neovascularization (mCNV) CONTRAINDICATIONS CIMERLI® is contraindicated in patients with ocular or periocular infections or known hypersensitivity to ranibizumab products or any of the excipients in CIMERLI®. Hypersensitivity reactions may manifest as severe intraocular inflammation WARNINGS AND PRECAUTIONS Endophthalmitis and Retinal Detachments: Intravitreal injections, including those with ranibizumab products, have been associated with endophthalmitis and retinal detachments. Proper aseptic injection technique should always be utilized when administering CIMERLI®. Patients should be monitored following the injection to permit early treatment, should an infection occur Increases in Intraocular Pressure: Increases in intraocular pressure (IOP) have been noted both pre-injection and post-injection (at 60 minutes) with ranibizumab products. Monitor intraocular pressure prior to and following intravitreal injection with CIMERLI® and manage appropriately Thromboembolic Events: Although there was a low rate of arterial thromboembolic events (ATEs) observed in the ranibizumab clinical trials, there is a potential risk of ATEs following intravitreal use of VEGF inhibitors. ATEs are defined as nonfatal stroke, nonfatal myocardial infarction, or vascular death (including deaths of unknown cause) Neovascular (wet) age-related macular degeneration The ATE rate in the 3 controlled neovascular AMD studies during the first year was 1.9% (17 of 874) in the combined group of patients treated with 0.3 mg or 0.5 mg ranibizumab compared with 1.1% (5 of 441) in patients from the control arms. In the second year of Studies AMD-1 and AMD-2, the ATE rate was 2.6% (19 of 721) in the combined group of ranibizumab-treated patients compared with 2.9% (10 of 344) in patients from the control arms. In Study AMD-4, the ATE rates observed in the 0.5 mg arms during the first and second year were similar to rates observed in Studies AMD-1, AMD-2, and AMD-3 In a pooled analysis of 2-year controlled studies (AMD-1, AMD-2, and a study of ranibizumab used adjunctively with verteporfin photodynamic therapy), the stroke rate (including both ischemic and hemorrhagic stroke) was 2.7% (13 of 484) in patients treated with 0.5 mg ranibizumab compared to 1.1% (5 of 435) in patients in the control arms (odds ratio 2.2 [95% confidence interval (0.8-7.1)]) Macular edema following retinal vein occlusion The ATE rate in the 2 controlled RVO studies during the first 6 months was 0.8% in both the ranibizumab and control arms of the studies (4 of 525 in the combined group of patients treated with 0.3 mg or 0.5 mg ranibizumab and 2 of 260 in the control arms). The stroke rate was 0.2% (1 of 525) in the combined group of ranibizumab-treated patients compared to 0.4% (1 of 260) in the control arms Diabetic macular edema and Diabetic Retinopathy In a pooled analysis of Studies D-1 and D-2, the ATE rate at 2 years was 7.2% (18 of 250) with 0.5 mg ranibizumab, 5.6% (14 of 250) with 0.3 mg ranibizumab, and 5.2% (13 of 250) with control. The stroke rate at 2 years was 3.2% (8 of 250) with 0.5 mg ranibizumab, 1.2% (3 of 250) with 0.3 mg ranibizumab, and 1.6% (4 of 250) with control. At 3 years, the ATE rate was 10.4% (26 of 249) with 0.5 mg ranibizumab and 10.8% (27 of 250) with 0.3 mg ranibizumab; the stroke rate was 4.8% (12 of 249) with 0.5 mg ranibizumab and 2.0% (5 of 250) with 0.3 mg ranibizumab Fatal events in patients with diabetic macular edema and diabetic retinopathy at baseline: A pooled analysis of Studies D-1 and D-2 showed that fatalities in the first 2 years occurred in 4.4% (11 of 250) of patients treated with 0.5 mg ranibizumab, in 2.8% (7 of 250) of patients treated with 0.3 mg ranibizumab, and in 1.2% (3 of 250) of control patients. Over 3 years, fatalities occurred in 6.4% (16 of 249) of patients treated with 0.5 mg ranibizumab and in 4.4% (11 of 250) of patients treated with 0.3 mg ranibizumab. Although the rate of fatal events was low and included causes of death typical of patients with advanced diabetic complications, a potential relationship between these events and intravitreal use of VEGF inhibitors cannot be excluded ADVERSE REACTIONS Serious adverse events related to the injection procedure have occurred in <0.1% of intravitreal injections, including endophthalmitis, rhegmatogenous retinal detachment, and iatrogenic traumatic cataract In ranibizumab-treated patients compared with the control group, the most common ocular side effects included conjunctival hemorrhage, eye pain, vitreous floaters, and intraocular pressure. The most common non-ocular side effects included nasopharyngitis, anemia, nausea, and cough As with all therapeutic proteins, there is the potential for an immune response in patients treated with ranibizumab products. The clinical significance of immunoreactivity to ranibizumab products is unclear at this time Postmarketing Experience The following adverse reaction has been identified during post-approval use of ranibizumab products: Ocular: Tear of retinal pigment epithelium among patients with neovascular AMD *An interchangeable product (IP) is a biological product that is approved based on data demonstrating that it is highly similar to an FDA-approved reference product (RP) and that there are no clinically meaningful differences between the products; it can be expected to produce the same clinical result as the RP in any given patient; and if administered more than once to a patient, the risk in terms of safety or diminished efficacy from alternating or switching between use of the RP and IP is not greater than that from the RP without such alternation or switch. Interchangeability of CIMERLI® has been demonstrated for the condition(s) of use, strength(s), dosage form(s), and route(s) of administration described in its Full Prescribing Information. To report SUSPECTED ADVERSE REACTIONS, contact Coherus BioSciences, Inc. at 1-800-483-3692 or FDA at 1-800-FDA-1088 or . For additional Safety Information, please see CIMERLI® Full Prescribing Information available here. About Coherus BioSciences Coherus is a commercial-stage biopharmaceutical company focused on the research, development and commercialization of innovative immunotherapies to treat cancer. Coherus’ strategy is to build a leading immuno-oncology franchise funded with cash generated through net sales of its diversified portfolio of FDA-approved therapeutics. In 2021, Coherus in-licensed toripalimab, an anti-PD-1 antibody, in the United States and Canada. The BLA for toripalimab in combination with chemotherapy as treatment for recurrent or metastatic nasopharyngeal carcinoma is currently under review by the FDA. Coherus markets UDENYCA® (pegfilgrastim-cbqv), a biosimilar of Neulasta® (pegfilgrastim), and CIMERLI® (ranibizumab-eqrn), a biosimilar of Lucentis® (ranibizumab injection), in the U.S., and expects to launch the FDA-approved Humira® (adalimumab) biosimilar YUSIMRY™ (adalimumab-aqvh) in the U.S. in mid-2023. In January 2023, Coherus agreed to enter into definitive agreements providing for the acquisition of exclusive U.S. commercial rights to an Eylea® (aflibercept) biosimilar, FYB203, and plans to BLA for FYB203 in 2023. Forward-Looking Statements Except for the historical information contained herein, the matters set forth in this press release are forward-looking statements within the meaning of the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995, including, but not limited to, statements regarding Coherus’ ability to build its immuno-oncology franchise to achieve a leading market position; Coherus’ ability to generate cash; Coherus’ investment plans; Coherus’ expectations for the launch date of YUSIMRY™; Coherus’ expectations about entering into definitive agreements and closing on those agreements to acquire exclusive U.S. commercial rights to an Eylea® biosimilar; expectations about Coherus’ ability to BLA for an Eylea® biosimilar; and expectations that obtaining a Q-code for CIMERLI® may result in market conversion or accelerating growth for CIMERLI® in the future;. Such forward-looking statements involve substantial risks and uncertainties that could cause Coherus’ actual results, performance or achievements to differ significantly from any future results, performance or achievements expressed or implied by the forward-looking statements. Such risks and uncertainties include, among others, risks and uncertainties of coordinating a launch for a new biosimilar in a competitive marketplace; risks and uncertainties inherent in the clinical drug development process; risks relating to executing business transactions; risks related to our existing and potential collaboration partners; risks of the drug development position of Coherus’ competitors; the risks and uncertainties of the regulatory approval process, including the speed of regulatory review, international aspects of Coherus’ business, the timing of Coherus’ regulatory filings; the risk of FDA review issues; the risk that Coherus is unable to complete commercial transactions and other matters that could affect the availability or commercial potential of Coherus’ drug candidates; and the risks and uncertainties of possible litigation. All forward-looking statements contained in this press release speak only as of the date of this press release. Coherus undertakes no obligation to update or revise any forward-looking statements. For a further description of the significant risks and uncertainties that could cause actual results to differ from those expressed in these forward-looking statements, as well as risks relating to Coherus’ business in general, see Coherus’ Annual Report on Form 10-Q for the quarter ended September 30, 2022, filed with the Securities and Exchange Commission on November 8, 2022, including the section therein captioned “Risk Factors” and in other documents that Coherus files with the Securities and Exchange Commission. UDENYCA®, CIMERLI®, COHERUS Solutions™ and YUSIMRY™, whether or not appearing in large print or with the trademark symbol, are trademarks of Coherus, its affiliates, related companies or its licensors or joint venture partners, unless otherwise noted. Trademarks and trade names of other companies appearing in this press release are, to the knowledge of Coherus, the property of their respective owners. Please see Prescribing Information for CIMERLI® (ranibizumab-eqrn). Coherus Contact Information: Investor Contact: Marek Ciszewski, SVP Investor Relations IR@coherus.com Media Contact: Jodi Sievers, VP Corporate Communications media@coherus.com

Drug ApprovalClinical ResultImmunotherapy

100 Deals associated with Verteporfin

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KEGG	Wiki	ATC	Drug Bank
D01162	Verteporfin	S01LA01	DB00460

R&D Status

Approved

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Indication	Country/Location	Organization	Date
Histoplasmosis	United States	Bausch + Lomb Ireland Ltd.	30 Jun 2008
Myopia, Degenerative	European Union	CHEPLAPHARM Arzneimittel GmbH	27 Jul 2000
Myopia, Degenerative	Iceland	CHEPLAPHARM Arzneimittel GmbH	27 Jul 2000
Myopia, Degenerative	Liechtenstein	CHEPLAPHARM Arzneimittel GmbH	27 Jul 2000
Myopia, Degenerative	Norway	CHEPLAPHARM Arzneimittel GmbH	27 Jul 2000
Wet age-related macular degeneration	European Union	CHEPLAPHARM Arzneimittel GmbH	27 Jul 2000
Wet age-related macular degeneration	Iceland	CHEPLAPHARM Arzneimittel GmbH	27 Jul 2000
Wet age-related macular degeneration	Liechtenstein	CHEPLAPHARM Arzneimittel GmbH	27 Jul 2000
Wet age-related macular degeneration	Norway	CHEPLAPHARM Arzneimittel GmbH	27 Jul 2000
Age Related Macular Degeneration	United States	Bausch + Lomb Ireland Ltd.	12 Apr 2000
Choroidal Neovascularization	United States	Bausch + Lomb Ireland Ltd.	12 Apr 2000

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Glycogen Storage Disease Type II	Phase 3	Austria	Novartis AG	01 May 2007
Glycogen Storage Disease Type II	Phase 3	Belgium	Novartis AG	01 May 2007
Glycogen Storage Disease Type II	Phase 3	Denmark	Novartis AG	01 May 2007
Glycogen Storage Disease Type II	Phase 3	France	Novartis AG	01 May 2007
Glycogen Storage Disease Type II	Phase 3	Germany	Novartis AG	01 May 2007
Glycogen Storage Disease Type II	Phase 3	Hungary	Novartis AG	01 May 2007
Glycogen Storage Disease Type II	Phase 3	Italy	Novartis AG	01 May 2007
Glycogen Storage Disease Type II	Phase 3	Netherlands	Novartis AG	01 May 2007
Glycogen Storage Disease Type II	Phase 3	Poland	Novartis AG	01 May 2007
Glycogen Storage Disease Type II	Phase 3	Spain	Novartis AG	01 May 2007

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT03033225 (CTgov)	Phase 2	Pancreatic carcinoma non-resectable	13	Photodynamic Therapy+Verteporfin	gyofafecaz = jzfcinnyfw yqnkiygvsw (maucancijd, kzzsydqyia - hojdgdcbvj) View more	-	30 Jul 2025
ITVT-02 (SNO2021)	Phase 1/2	Glioblastoma EGFR \| PI3K	-	Verteporfin	odnifjivjr(llrmeuxlqv) = vmjpmttegy jelqkheifu (mzqkoqpqjx )	-	12 Nov 2021
				Verteporfin Photodynamic Therapy	odnifjivjr(llrmeuxlqv) = mygoxmhnzd jelqkheifu (mzqkoqpqjx )
NCT03033225 (Pubmed \| Gastrointest Endosc)	Phase 2	Pancreatic Cancer	8	EUS-guided verteporfin PDT	qbdevytxrv(pgyurndnfc) = gjwrqonrja wlkacmtlrq (zsgohufnyd ) View more	Positive	26 Feb 2021
AAO2020	Not Applicable	Uveal Melanoma	26	Primary PDT with Verteporfin	pmgibkoeno(ktmlgnsjts) = ovzgolwmgr xdtcqbfylh (koujcckfvh )	Negative	13 Nov 2020
NCT01846273 (EVEREST II, CTgov)	Phase 4	Age Related Macular Degeneration \| Polypoidal choroidal vasculopathy	321	Ranibizumab (Ranibizumab 0.5 mg + vPDT)	shwkatqcry(iylhcphqjc) = nckxiodchq gzlotrhfba (kvktcwipof, 1.00) View more	-	07 Jun 2019
				Ranibizumab (Ranibizumab 0.5 mg)	shwkatqcry(iylhcphqjc) = lrbmbupvbt gzlotrhfba (kvktcwipof, 1.06) View more
NCT02120950 (PLANET, CTgov)	Phase 4	Wet age-related macular degeneration \| Polypoidal choroidal vasculopathy	333	Visudyne+Aflibercept (Eylea, VEGF Trap-Eye, BAY86-5321) (Aflibercept + Active PDT)	mpwxudoabq(glssiszsfi) = awpvtpoaow kfcswmirxc (coytnnfguw, 10.7) View more	-	15 Jan 2019
				Aflibercept (Eylea, VEGF Trap-Eye, BAY86-5321) (Aflibercept + Sham PDT)	mzfiqjugdj(zwnclgoqey) = cdslcdlsez cpfqmqtxii (xxbesytoup, zqoxuwxgyn - ctpfuawpzq) View more
NCT01846273 (EVEREST II, ARVO2018)	Phase 4	Polypoidal choroidal vasculopathy	322	Ranibizumab 0.5 mg combined with verteporfin photodynamic therapy	rmaxgcnsvd(wlaqrzlynw) = guptdanfom nhllpfgikm (xhdiqltfdt ) View more	Positive	01 Jul 2018
				Ranibizumab 0.5 mg monotherapy	rmaxgcnsvd(wlaqrzlynw) = brrxwopqbf nhllpfgikm (xhdiqltfdt ) View more
NCT01846273 (Pubmed \| JAMA Ophthalmol) Manual	Phase 4	Polypoidal choroidal vasculopathy	322	verteporfin photodynamic therapy +Ranibizumab	uupnrburul(hrelabtwxx) = bqcgewqyls sdvtzysatb (uafstkltfq ) View more	Positive	01 Nov 2017
				Ranibizumab	uupnrburul(hrelabtwxx) = ousywztthy sdvtzysatb (uafstkltfq ) View more
ARVO2017 Manual	Not Applicable	Wet age-related macular degeneration	16	Adjunctive Indocyanine Green Angiography-Directed Verteporfin Photodynamic Therapy	emmomslfeb(yzwyusdywk) = vyjimqypys nyehwdmpvp (pmolyrdqbr )	Positive	01 Jun 2017
NCT01846273 (EVEREST II, ARVO2017)	Phase 4	Polypoidal choroidal vasculopathy	492	ranibizumab + verteporfin photodynamic therapy	jroepjjmyw(siiyyzlain) = afsbadltiw sjrszwiksh (vsypxluhay ) View more	-	01 Jun 2017
				ranibizumab monotherapy	jroepjjmyw(siiyyzlain) = smofpokvjk sjrszwiksh (vsypxluhay ) View more

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