M-CSF and G-CSF Inhibitor Composition for Pulmonary Fibrosis

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Solution Overview

Problem

Current treatments and biomarkers for pulmonary fibrosis, particularly induced by radiation therapy, are inadequate in effectively preventing or diagnosing the condition, and there is a lack of effective therapeutic agents using M-CSF and G-CSF inhibitors.

Innovation Solution

A composition comprising M-CSF and G-CSF inhibitors, specifically anti-M-CSF and anti-G-CSF antibodies, is used to inhibit myofibroblast hyperplasia and pulmonary fibrosis by blocking the differentiation of pulmonary cells into myofibroblasts and reducing extracellular matrix remodeling, along with a diagnostic marker using M-CSF and G-CSF expression levels.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If radiation therapy is used to treat lung cancer and breast cancer, then cancer treatment effectiveness is improved, but pulmonary fibrosis is induced as a side effect

Engineering Contradiction:
Improvecancer treatment effectivenessVSAvoidpulmonary fibrosis
Core Design Contradiction:
ReliabilityVSObject-affected harmful factors

Solution Approach 1:

The patent applies preliminary anti-action by administering M-CSF and G-CSF inhibitors before or during radiation therapy to prevent the induction of pulmonary fibrosis. The composition blocks the differentiation of pulmonary cells into myofibroblasts and reduces extracellular matrix remodeling in advance, thereby preventing the harmful fibrotic response while allowing the cancer treatment to proceed effectively.

Inventive Principle:
Principle #9Preliminary anti-action

Solution Approach 2:

The patent uses M-CSF and G-CSF inhibitors as intermediary substances that mediate between the radiation therapy and the pulmonary tissue. These inhibitors interfere with the signaling pathways that lead to myofibroblast differentiation and extracellular matrix accumulation, thereby protecting the lung tissue from radiation-induced fibrosis while maintaining the therapeutic effect on cancer.

Inventive Principle:
Principle #24Intermediary (Mediator)

2Reliability

If existing therapeutic agents such as TGF-β and IFN-γ are used for fibrotic diseases, then some therapeutic effect is achieved, but the effect is not sustainable due to various signals in the human body

Engineering Contradiction:
Improvetherapeutic effectVSAvoidsustainability of therapeutic effect
Core Design Contradiction:
ReliabilityVSDuration of action of stationary object

Solution Approach 1:

The patent changes the therapeutic parameters by switching from using TGF-β and IFN-γ (which are affected by various conflicting signals in the body) to using M-CSF and G-CSF inhibitors. This parameter change targets specific cytokine pathways that are more consistently involved in the fibrotic process, thereby achieving a more sustainable therapeutic effect. The inhibitors specifically block M-CSF and G-CSF signaling, which are key drivers of myofibroblast differentiation and extracellular matrix remodeling.

Inventive Principle:
Principle #35Parameter changes

3Measurement precision

If studies on M-CSF or G-CSF biomarker use are conducted, then diagnostic capability is improved, but insufficient research has been done on mixed antibody targeting both factors

Engineering Contradiction:
Improvediagnostic capabilityVSAvoidresearch completeness
Core Design Contradiction:
Measurement precisionVSDevice complexity

Solution Approach 1:

The patent merges the targeting of M-CSF and G-CSF into a single composition containing both inhibitors. This combined approach provides a more comprehensive diagnostic and therapeutic tool compared to studying each factor separately. The mixed antibody composition simultaneously blocks both M-CSF and G-CSF pathways, offering a more complete intervention strategy for pulmonary fibrosis while improving diagnostic capability through the evaluation of both biomarkers.

Inventive Principle:
Principle #5Merging (Combining)

Applied Scientific Principles

This section explains which scientific principles are used to turn an abstract innovation direction into a practical engineering solution.

Function Achieved in This Case

The composition significantly inhibits myofibroblast hyperplasia and pulmonary fibrosis, providing a reliable diagnostic tool for the condition and a therapeutic approach to prevent or treat pulmonary fibrosis.

Implementation Method 1

a composition for preventing or treating pulmonary fibrosis, comprising an M-CSF inhibitor and a G-CSF inhibitor as active ingredients

Methodology Applied
Scientific EffectAntibody blocking:

Implementation Method 2

inhibit myofibroblast hyperplasia and pulmonary fibrosis by blocking the differentiation of pulmonary cells into myofibroblasts and reducing extracellular matrix remodeling

Methodology Applied
Scientific EffectInhibition of cell differentiation:

Data Source

PatentUS20250376515A1Use of m-CSF or g-CSF for diagnosis or treatment of pulmonary fibrosis
Publication Date: 2025.12.11 FNCT BIOTECH INC
  • US20250376515A1 patent drawing
  • US20250376515A1 patent drawing
  • US20250376515A1 patent drawing

AI summary

The present disclosure relates to a use of M-CSF or G-CSF for diagnosis or treatment of pulmonary fibrosis and, more specifically, to: a marker for diagnosing the level of development or progression of pulmonary fibrosis, comprising M-CSF and/or G-CSF; and a composition for preventing or treating pulmonary fibrosis, comprising an M-CSF inhibitor and a G-CSF inhibitor as active ingredients.The present inventors have ascertained that M-CSF and/or G-CSF is a marker for development or progression of pulmonary fibrosis, and have confirmed that a composition, which comprises M-CSF and G-CSF and which binds to M-CSF and G-CSF so that the inherent mechanism thereof can be prevented, has an effect of significantly inhibiting myofibroblast hyperplasia or pulmonary fibrosis of the pulmonary cells, and thus the marker and the composition of the present disclosure are expected to be effectively usable for diagnosis, prevention or treatment of pulmonary fibrosis.