Fndc5 Secreted Polypeptides for Brown Fat Induction

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Solution Overview

Problem

Current therapies for metabolic disorders such as diabetes and obesity are ineffective, and there is a lack of identified molecular regulators and diagnostic, prognostic, and therapeutic agents to manage these conditions effectively.

Innovation Solution

The use of Fndc5 and biologically active fragments thereof, which are secreted polypeptides that induce significant induction of brown fat cells at nanomolar concentrations, modulating metabolic responses and treating metabolic disorders by inducing expression of specific genes and improving insulin sensitivity, thermogenesis, and reducing obesity and diabetes.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If current therapies are used for metabolic disorders, then treatment is provided, but the therapies are ineffective

Engineering Contradiction:
Improvetherapeutic effectivenessVSAvoidlack of molecular regulators
Core Design Contradiction:
ReliabilityVSAdaptability or versatility

Solution Approach 1:

The patent uses PGC1α as an intermediary molecule that mediates the effect of exercise on brown fat induction. PGC1α is identified as the key molecular regulator that translates mechanical exercise into biochemical changes, specifically inducing UCP1 expression and brown fat thermogenesis. This intermediary approach resolves the contradiction by providing a specific molecular mechanism that current general therapies lack.

Inventive Principle:
Principle #24Intermediary (Mediator)

Solution Approach 2:

The patent employs preliminary action by using exercise or PGC1α induction before metabolic disorders fully develop. The approach of inducing brown fat through exercise or PGC1α activation in advance creates a protective metabolic state that prevents or treats insulin resistance and type 2 diabetes before they manifest clinically.

Inventive Principle:
Principle #10Preliminary action

2Reliability

If exercise is performed to induce PGC1α, then beneficial metabolic effects are achieved, but the mechanism and specific factors remain unidentified

Engineering Contradiction:
Improvemetabolic benefitsVSAvoid unidentified molecular factors
Core Design Contradiction:
ReliabilityVSLoss of information

Solution Approach 1:

The patent extracts and identifies PGC1α as the specific molecular factor responsible for mediating exercise benefits. By isolating PGC1α as the key regulator that connects exercise to brown fat induction and metabolic improvement, the patent converts the general observation of exercise benefits into a specific, identifiable molecular mechanism that can be targeted therapeutically.

Inventive Principle:
Principle #2Taking out (Extraction)

3Productivity

If no specific molecular regulators are identified, then research continues, but effective therapies cannot be developed

Engineering Contradiction:
Improveresearch progressVSAvoidtherapeutic development
Core Design Contradiction:
ProductivityVSReliability

Solution Approach 1:

The patent identifies PGC1α as the critical intermediary molecule that bridges exercise and metabolic health. This specific molecular regulator serves as a tangible target for drug development and therapeutic intervention, converting abstract research concepts into actionable therapeutic strategies for treating insulin resistance and type 2 diabetes.

Inventive Principle:
Principle #24Intermediary (Mediator)

Data Source

PatentUS11098092B2Compositions and methods for brown fat induction and activity using FNDC5
Publication Date: 2021.08.24 DANA FARBER CANCER INSTITUTE INC
  • US11098092B2 patent drawing
  • US11098092B2 patent drawing
  • US11098092B2 patent drawing

AI summary

The invention provides compositions and methods for brown fat induction and activity through modulation of Fndc5 activity and/or expression. Also provided are methods for preventing or treating metabolic disorders in a subject through modulation of Fndc5 activity and/or expression. Further provided are methods for identifying compounds that are capable of modulating Fndc5 activity and/or expression.