#jnj 61186372

[impossibledeanmakerwombat]

Intratumoral Cancer Therapies Market to Latest Research, Industry Analysis, Driver, Trends, Business Overview, Key Value, Demand And Forecast 2023 to 2032

A recently published study by FMI expects the global Intratumoral Cancer Therapies market to garner a market value of US$ 212.96 Billion in 2023 and is expected to accumulate a market value of US$ 552.36 Billion by registering a CAGR of 10% in the forecast period 2023-2033.

Growth of the Intratumoral Cancer Therapies market can be attributed to favorable regulatory frameworks for cancer treatments. The market for Intratumoral Cancer Therapies registered a CAGR of 7% in the historical period 2017-2022.

The growth is attributed to the increasing prevalence of cancer cases, pushing the regulatory bodies to work on research and development. For instance, in September 2022, the Hadassah Cancer Research Institute (HCRI), Jerusalem declared that it will lead the CancerRNA, a global forum working towards development and application of RNA-based immunotherapy to effectively utilize anti-cancer immune responses.

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In terms of market share and revenue, the North American market is predicted to be the most lucrative market during the forecast period with a revenue share of 40%. The region’s growth is driven by the presence of various biotechnology and medical device firms. For instance, in March 2020, Johnson and Johnson received the US FDA Breakthrough Therapy Designation for JNJ-61186372 (JNJ-6372) for the treatment of patients with metastatic non-small cell lung cancer (NSCLC).

Key Takeaways from the Market Study

From 2017-2022, the Intratumoral Cancer Therapies market grew at CAGR of 7%.

The global Intratumoral Cancer Therapies market is expected to grow with a 10% CAGR during 2023-2033.

As of 2033, the Intratumoral Cancer Therapies market is expected to reach US$ 552.36 Billion.

Checkpoint inhibitors segment is poised to register the highest growth rate through 2033.

North America is expected to possess 40% market share for Intratumoral Cancer Therapies market in North America.

The European market is predicted to increase significantly throughout the forecast period, with a CAGR of 5% during the forecast period.

By application, lung cancer is estimated to account for the largest share of the market.

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“Cancer is among the top causes of mortality worldwide, and its incidence is increasing at an alarming rate. As a result, healthcare experts are concentrating on the development of efficient treatment and diagnosis solutions in order to reduce the incidence level.” says an FMI analyst

Market Competition

Key players in the Intratumoral Cancer Therapies market are Amgen Inc, AstraZeneca, Bayer AG, Bristol-Myers Squibb Company, Pfizer Inc, Novarts AG, Johnson & Johnson, and Eli Lily Company, F.

Gland Pharma has launched the cancer treatment medicine Bortezomib for Injection in the United States in 2022. The drug business stated in a statement that it has released the medicine in the US market through a partner who has acquired permission from the US Food and Drug Administration (USFDA). The business claims that its medicine is medically similar to Velcade for Injection from Takeda Pharmaceuticals. Bortezomib for Intravenous is used to treat cancers such as myeloma and mantle cell lymphoma.

Key Segments Profiled in the Intratumoral Cancer Therapies Industry Survey

Technology:

Monoclonal Antibodies

Vaccines

Checkpoint Inhibitors

Cell Therapies

Immune System Modulators

Adoptive Cell Transfer

Cytokines

Application:

Lung Cancer

Breast Cancer

Melanoma

Prostate Cancer

Head & Neck Cancer

Others

End-users:

Hospitals

Cancer Research Centres

Clinics

Full Report @ https://www.futuremarketinsights.com/reports/intratumoral-cancer-therapies-market

[pharmaphorumuk]

Janssen/Genmab antibody could be lung cancer breakthrough

The FDA thinks a dual-target antibody from Janssen and development partner Genmab could set new standards in treatment for certain patients with lung cancer, whose disease has progressed after chemotherapy and are unlikely to respond to commonly used alternatives.

The regulator said that the Johnson & Johnson unit’s JNJ-61186372 (JNJ-6372) could be a Breakthrough Therapy for patients with metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) Exon 20, whose disease has progressed on or after platinum-based chemotherapy.

JNJ-6372 is an EGFR-mesenchymal epithelial transition factor (MET) bispecific antibody that targets activating and resistant EGFR and MET mutations and amplifications.

There are no FDA-approved targeted therapies for patients with lung cancer who have EGFR Exon 20 insertion mutations.

This group of patients have a form of the disease that is generally insensitive to EGFR tyrosine kinase inhibitor (TKI) therapy such as AstraZeneca’s Iressa (gefitinib) and Roche’s Tarceva (erlotinib).

The FDA reserves Breakthrough Therapy status for therapies that could represent a significant improvement over standard of care – in this case conventional chemotherapy – in either efficacy, safety, or both.

Drugs with this tag get extra support from the FDA during clinical development and it paves the way for a faster six-month review once an evidence dossier has been filed.

The Breakthrough Therapy Designation is supported by data from a phase 1, first-in-human, open-label, multicentre study, which evaluates the safety, pharmacokinetics and preliminary efficacy of JNJ-6372 as monotherapy and in combination with a third-generation EGFR TKI, lazertinib.

This study will determine the recommended dose for patients in a phase 2 trial with advanced NSCLC.

Enrolment into part 2 dose expansion cohorts is ongoing as the study tests JNJ-6732 monotherapy in multiple NSCLC sub-populations with genomic alternations such as those with C7975 resistance mutation or MET amplification.

Production and development of the antibody followed Janssen’s licensing agreement with Genmab for use of its DuoBody technology platform.

The post Janssen/Genmab antibody could be lung cancer breakthrough appeared first on .

from https://pharmaphorum.com/news/janssen-genmab-antibody-could-be-lung-cancer-breakthrough/

[cancersfakianakis1]

Characterization of In Vivo Resistance to Osimertinib and JNJ-61186372, an EGFR/Met Bispecific Antibody, Reveals Unique and Consensus Mechanisms of Resistance

Approximately 10% of non–small cell lung cancer (NSCLC) patients in the United States and 40% of NSCLC patients in Asia have activating epidermal growth factor receptor (EGFR) mutations and are eligible to receive targeted anti-EGFR therapy. Despite an extension of life expectancy associated with this treatment, resistance to EGFR tyrosine kinase inhibitors and anti-EGFR antibodies is almost inevitable. To identify additional signaling routes that can be cotargeted to overcome resistance, we quantified tumor-specific molecular changes that govern resistant cancer cell growth and survival. Mass spectrometry–based quantitative proteomics was used to profile in vivo signaling changes in 41 therapy-resistant tumors from four xenograft NSCLC models. We identified unique and tumor-specific tyrosine phosphorylation rewiring in tumors resistant to treatment with the irreversible third-generation EGFR-inhibitor, osimertinib, or the novel dual-targeting EGFR/Met antibody, JNJ-61186372. Tumor-specific increases in tyrosine-phosphorylated peptides from EGFR family members, Shc1 and Gab1 or Src family kinase (SFK) substrates were observed, underscoring a differential ability of tumors to uniquely escape EGFR inhibition. Although most resistant tumors within each treatment group displayed a marked inhibition of EGFR as well as SFK signaling, the combination of EGFR inhibition (osimertinib) and SFK inhibition (saracatinib or dasatinib) led to further decrease in cell growth in vitro. This result suggests that residual SFK signaling mediates therapeutic resistance and that elimination of this signal through combination therapy may delay onset of resistance. Overall, analysis of individual resistant tumors captured unique in vivo signaling rewiring that would have been masked by analysis of in vitro cell population averages. Mol Cancer Ther; 16(11); 2572–85. ©2017 AACR.

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#Oncology-Sfakianakis

[cancersfakianakis1]

Characterization of in vivo resistance to osimertinib and JNJ-61186372, an EGFR/Met bi-specific antibody, reveals unique and consensus mechanisms of resistance

Approximately 10% of non-small cell lung cancer (NSCLC) patients in the U.S. and 40% of NSCLC patients in Asia have activating EGFR mutations and are eligible to receive targeted anti-EGFR therapy. Despite an extension of life expectancy associated with this treatment, resistance to EGFR tyrosine kinase inhibitors and anti-EGFR antibodies is almost inevitable. To identify additional signaling routes that can be co-targeted to overcome resistance, we quantified tumor-specific molecular changes that govern resistant cancer cell growth and survival. Mass spectrometry-based quantitative proteomics was used to profile in vivo signaling changes in 41 therapy resistant tumors from four xenograft NSCLC models. We identified unique and tumor-specific tyrosine phosphorylation rewiring in tumors resistant to treatment with the irreversible third generation EGFR-inhibitor, osimertinib, or the novel dual-targeting EGFR/Met antibody, JNJ-61186372. Tumor-specific increases in tyrosine-phosphorylated peptides from EGFR family members, Shc1 and Gab1 or Src family kinase substrates were observed, underscoring a differential ability of tumors to uniquely escape EGFR inhibition. Although most resistant tumors within each treatment group displayed a marked inhibition of EGFR as well as Src family kinase (SFK) signaling, the combination of EGFR inhibition (osimertinib) and SFK inhibition (saracatinib or dasatinib) led to further decrease in cell growth in vitro. This result suggests that residual SFK signaling mediates therapeutic resistance and that elimination of this signal through combination therapy may delay onset of resistance. Overall, analysis of individual resistant tumors captured unique in vivo signaling rewiring that would have been masked by analysis of in vitro cell population averages.

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#Oncology-Sfakianakis