Remember When Blood Sugar Control Wasn’t Something You Had to Think About?
It was a time when your β-cells could keep up with your body’s insulin needs or were even strong enough to overcome insulin resistance.
In type 2 diabetes, our β-cells and medications work together to compensate for insulin resistance. Over time, as β-cell function declines, we need more medication to compensate for the lost β-cell function.
This is how blood sugar becomes harder to control.
What Are the Signs of Declining β-Cell Function?
Adults 40+ with blood sugar management issues.
- Human studies show an age-associated decline in β-cell function, with measurable differences emerging between younger and older-than-40 populations. (1,2)
Normal body weight but needing blood sugar support.
- Lean T2D is often associated with more pronounced insulin deficiency and β-cell dysfunction than insulin sensitivity issues. (3,4)
Newly diagnosed type 2 diabetes.
- By the time T2D is clinically diagnosed, only 50% of β-cell function remains at diagnosis and continues to decline at a rate of 5% annually. (5)
The progression of T2D.
- While insulin resistance is an early hallmark, longitudinal studies show that once diabetes is established, the continuous worsening of blood sugar control is mainly due to the steady decline in β-cell function. (6)
Can β-cells Regain Their Function?
We have known for years that "Upon recovery from (ER) stress, β-cells regain their identity and function, indicating a high degree of adaptive plasticity". (7)
The message is clear:
β-cell dysfunction does not always mean that the cells have permanently lost their ability to function.
The question is:
Can we reduce cellular stress to help β-cells function better?
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Can Cellular Stress Be Reduced?
Synthesized compounds such as KM04794, 4-PBA, and others have shown that reducing cellular stress can improve β-cell resilience and function. (8,9)
These studies support an important principle:
The cellular environment, especially the stress level, within β-cells can influence how well they function.
Servo BioLabs took a different route—searching botanical sources for naturally derived compounds that modulate the cell's own stress-regulation system - Endoplasmic Reticulum Associated Degradation (ERAD).
Our research identified TX-107 and related ERAD modulators and uses them as ERAD Plus ingredients.
ERAD Plus Pre-D
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Naturally supports cellular stress balance
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Supports the body’s natural glucose-regulation processes
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Trusted since 2018
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90-day money-back guarantee
You Should Know How It Works
TX-107 and related compounds are studied as ERAD modulators.
ERAD is a cellular cleanup system that identifies and removes misfolded proteins from the ER (Endoplasmic Reticulum).
When these misfolded proteins accumulate, they cause cellular stress (specifically, ER stress) and disrupt normal β-cell function.
The strategy is simple:
Enhance ERAD → reduce the misfolded-protein burden that causes cellular stress → improve β-cell function.
We Didn’t Start With Ingredients.
We Started With a Cellular Target.
Most supplements start by combining ingredients believed to support blood sugar (the symptom).
We use a completely different approach:
Identify the cellular problem — excessive ER stress
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Find the target — ERAD, the system that removes misfolded proteins that cause ER stress
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Search experimentally for natural ERAD modulators
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Validate their function in supporting β-cells in cells, animals, and humans
This logical, experiment-driven research approach became the foundation of ERAD Plus Pre-D.
ERAD Plus® Supports the β-Cell’s Natural ERAD System
Not “Adding More,” but Removing What Shouldn’t Be There.
ERAD Plus was developed around a simple idea:
Support the cell's own cleanup system and help maintain the cellular environment β-cells need to do their normal job.
Try ERAD Plus Pre-D for 90 Days,
Risk-free
Simply send us a message with the order number if you are not fully satisfied for any reason. We will issue you a full refund.
References:
1. Functional changes in beta cells during ageing and senescence. Diabetologia. 2020 Oct;63(10):2022-2029.
2. Pancreatic β-cell aging in physiology and diabetes: emerging roles of m6A mRNA methylation. J Mol Endocrinol. 2026; 77(1):e250159.
3. Lean type 2 diabetes: the overlooked epidemic reshaping global health. Diabetol Metab Syndr. 2025 Nov 26;17(1):440.
4. Lean diabetes is one end of the spectrum of type 2 diabetes and not a separate entity. Diabetes Res. Clin. Pract. 2025; 227: 112387
5. Multi-phases of islet beta-cell function change in type 2 diabetes mellitus and its influencing factors. Front. Endocrinol. 16:1602796.
6. Reversing pancreatic β-cell dedifferentiation in the treatment of type 2 diabetes. Exp Mol Med. 2023; 55, 1652–1658.
7. Adaptation to chronic ER stress enforces pancreatic β-cell plasticity. Nat Commun 13, 4621 (2022)
8. Identification of an endoplasmic reticulum proteostasis modulator that enhances insulin production in pancreatic β cells. Cell Chem Biol. 2022 Jun 16;29(6):996-1009
9. Use of Small Organic Molecules to Improve Pancreatic Beta Cell Resilience to IAPP-Induced Proteotoxic Stress. Int. J. Mol. Sci. 2026, 27, 3004.