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yellowpigment.com · Confidential · 2026
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Seed Round · Confidential · 2026
Turning a protective
human phenotype
into medicine.
Therapeutics for inflammatory and metabolic disease(s), built on the natural protective biology of Gilbert syndrome.
Human genetics-inspired drug discovery · Biliverdin-ester prodrug platform
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The Opportunity

Major inflammatory and metabolic diseases
remain poorly served.

Many chronic conditions still lack therapies that are both mechanistically differentiated and suitable for durable, broad disease modification.

Inflammatory Disease
Chronic inflammation at scale

Anti-phospholipid syndrome (APS) remains without FDA-approved disease-modifying therapy beyond anticoagulation

Systemic inflammatory conditions affect tens of millions globally, with significant morbidity and treatment gaps

Existing treatments target downstream pathways. Few address the underlying oxidative and inflammatory biology

Metabolic Disease
Metabolic dysfunction is epidemic

Obesity, metabolic syndrome, and cardiometabolic risk affect over a billion people globally

Inflammatory and metabolic dysfunction are tightly linked, driven by shared oxidative stress pathways

Chronic low-grade inflammation ("inflammaging") is a central driver of age-related functional decline.

There is a better target hiding in human biology itself.
The Opportunity

Gilbert syndrome is a well-documented natural experiment
in protective biology.

Gilbert syndrome, a benign, common genetic variant of UGT1A1 carried by ~5–10% of the population, produces mildly elevated unconjugated bilirubin. Decades of human epidemiology, across multiple independent cohorts, show consistent protection across major disease domains.

−50%
All-cause mortality
In Gilbert syndrome vs. age-matched population controls, large UK cohort study
Horsfall LJ et al. 2013 · n > 2,000
−60%
Coronary heart disease risk
In UGT1A1*28 homozygotes vs. wildtype, Framingham Heart Study cohort
Lin JP et al. · Framingham
Lower BMI & fat mass
Metabolic phenotype
Gilbert-range bilirubin associated with lower adiposity and waist circumference, especially in adults ≥ 35 years
Seyed Khoei N et al. 2018 · Free Radic Biol Med
Inflammatory protection
Autoimmune signal
Lower bilirubin tracks with elevated APS inflammatory burden. Elevated BR may confer protection in autoimmune states
Multiple cohort studies
Key Insight
Nature has already run the experiment — mild bilirubin elevation is consistently protective across mortality, cardiovascular, metabolic, and inflammatory disease.
The Science

A validated human pathway can be
translated into medicine.

The bilirubin pathway offers a translational bridge from human genetics to pharmacology, with a clear molecular target, an understood mechanism, and a defined therapeutic window with substantial safety margin.

Precursor
Heme
HO-1 / HO-2
Intermediate
Biliverdin
BLVRA / BLVRB
⭑ Therapeutic Target
Bilirubin
⚑ Gilbert protective window
UGT1A1
↓ in Gilbert
Excreted
BR-Glucuronide
Bilirubin Concentration by Clinical State Plasma bilirubin (µM)
Normal
3.4 – 17 µM
Gilbert protective window
★ YPT therapeutic window
15 – 100 µM
Crigler-Najjar II
100 – 350 µM
Crigler-Najjar I
350 – 900 µM
Normal
★ YPT therapeutic window ★ YPT
CN-II
CN-I
0
15
100
350
900
µM →
Safety Margin
From the upper bound of the YPT window (~100 µM) to severe hyperbilirubinemia (~350 µM CN-II), there is a ~3.5× distance, substantial pharmacological headroom for controlled bilirubin elevation.
The goal is not hyperbilirubinemia. It is controlled access to the Gilbert protective window with a wide safety margin.
The Science

Bilirubin biology explains
the Gilbert protective phenotype.

The protection observed in Gilbert syndrome is not coincidence. It is mechanistically driven. Mildly elevated bilirubin acts through four convergent biological axes that together explain the breadth of protection seen across mortality, cardiovascular, metabolic, and inflammatory disease.

01
PPARα Modulation
Bilirubin acts as an endogenous PPARα ligand, activating fatty acid oxidation and regulating lipid homeostasis. This is the mechanistic basis for metabolic protection in Gilbert individuals.
Metabolic axis
02
Lipophilic Antioxidant
BR intercepts peroxyl radicals in lipid membranes, a compartment inaccessible to water-soluble antioxidants. The BV → BR → BV redox cycle amplifies capacity beyond stoichiometric ratios.
Oxidative stress
03
BLVRA Signaling
Biliverdin reductase A is a dual-function kinase. Beyond BV reduction, it modulates insulin receptor signaling (IRS-1/PI3K) and NFκB, placing it centrally in metabolic and inflammatory control.
Signaling axis
04
Microbial Modulation
BV and BR exhibit anti-viral and anti-bacterial activity at epithelial barriers, supporting immune homeostasis. Emerging evidence links Gilbert-range BR to favourable host-microbial interaction profiles.
Host–microbiome axis
Four convergent biological mechanisms explain the Gilbert protective phenotype — and define the molecular targets a bilirubin-elevating therapy can engage. 5–10% global Gilbert carrier rate · 4 convergent mechanisms
Platform

Why bilirubin has not yet become
a practical drug.

The therapeutic signal is real. But bilirubin itself has been difficult to translate into a scalable, orally delivered medicine.

01 — Signal
Compelling biology
Strong epidemiological evidence across mortality, cardiovascular, metabolic, and inflammatory disease. Multiple mechanisms. Clear human phenotype. The biology works.
Validated in humans
→
02 — Problem
Delivery bottleneck
Bilirubin itself is chemically difficult. Most published attempts use injectable, infusion, or nanoparticle approaches that limit utility for chronic disease.
A.Poor aqueous solubility
B.Chemical instability
C.Hard formulation
D.Rapid degradation by gut microbiome
→
03 — Opportunity
Oral prodrug strategy
A drug design strategy that masks the problematic chemical features of bilirubin while preserving access to its biology. Delivered orally. Suitable for chronic use.
YPT's approach
The challenge has not been whether bilirubin biology matters. The challenge has been making it druggable.
Platform

Yellow Pigment is building
biliverdin-ester prodrugs.

Biliverdin-esters are a practical drug design strategy to access bilirubin biology in a tractable, developable format suitable for oral delivery and chronic use.

BV-Ester
Prodrug
Oral dose
GI lumen
Esterase
Biliverdin
BV
Absorbed
Systemic
BLVRA/B
Bilirubin
BR
Active
Pharmacology
UGT1A1
Therapeutic
Effect
Gilbert-range
biology
Improved absorption
Ester groups increase lipophilicity, enabling passive GI uptake
Endogenous activation
Esterases regenerate BV → BLVRA/B converts to BR
Better CMC profile
Improved formulation path vs. bilirubin free acid
IP-protected space
Ester design creates proprietary composition-of-matter opportunity
A chemistry strategy designed for druggability, oral delivery, and mechanistic relevance.
Platform

Early evidence supports
platform plausibility.

Published and internal data support that biliverdin-ester constructs can improve membrane permeability and convert through the intended biological pathway.

Published Precedent
BV dimethyl ester (BV-Me₂) demonstrates improved membrane passage versus unmodified biliverdin in published permeability studies
BV-Me₂ is a substrate for serum and cellular esterases in vitro and in vivo, supporting the bioactivation mechanism
Epidemiological evidence across four independent study cohorts confirms the human protective phenotype
Internal Readouts
Extracellular BV-to-BR conversion confirmed in monocyte cell culture, demonstrating biologically relevant conversion
BLVRA knockout slows BV-to-BR conversion, confirming enzymatic mechanism and pathway specificity
HPLC, fluorescence (iRFP/eUnaG) and permeability assays developed to support compound screening and lead selection
The platform has an early mechanistic and translational signal — not just a theoretical idea.
Pipeline

One engine,
multiple programs.

A single chemistry and biology platform generates multiple disease programs targeting some of medicine's largest and most persistent chronic disease markets.

Clinical Entry
Inflammatory / APS
Focused orphan indication with clear mechanism and development path
Standard-of-care treatment remains poorly defined in important APS settings, with no approved disease-modifying therapy beyond anticoagulation
Human APS data directly supports mechanistic hypothesis
Market Opportunity
Orphan
Focused entry · credible bridge to $100B+ autoimmune & cardiometabolic adjacencies
Lead Program
Metabolic / Obesity
PPARα agonism and antioxidant activity, established mechanisms linked to lower adiposity and improved metabolic health
GLP-1 adjunct positioning for lifelong weight control
Gilbert epidemiology: lower BMI, better adiposity
Market Opportunity
>1B
patients worldwide · multi-$10B+ annual obesity & metabolic market
Expansion
Inflammatory & Tissue Repair
Broader oxidative and inflammatory disease settings
Cross-applicable screening, tox, and translational learnings
Candidate-specific optimization via HTS library
Market Opportunity
$100B+
annual autoimmune & inflammatory disease market
One platform targeting major chronic-disease markets through an oral, once-daily format suited to long-duration therapy.
Pipeline

APS as the first clinical wedge.
Metabolic / Obesity as the lead commercial program.

APS is an attractive initial indication, strongly connected to inflammatory and oxidative stress biology, with a focused development path. Metabolic / Obesity is the large commercial opportunity the platform is designed to reach.

Clinical Entry
Anti-Phospholipid Syndrome (APS)
A systemic autoimmune condition characterized by thrombosis, inflammatory burden, and elevated oxidative stress. No approved disease-modifying therapy exists beyond anticoagulation.
Orphan potential Focused entry
  • Human data in APS links lower bilirubin with higher inflammatory burden, with direct mechanistic relevance
  • Mechanism aligns with anti-inflammatory and cytoprotective biology of the BV-ester platform
  • Small, focused indication with a clear regulatory path vs. launching directly into broad metabolic markets
Lead Commercial Program
Metabolic / Obesity: GLP-1 Adjunct
A lifelong weight-control therapy positioned alongside incretin-based drugs. PPARα-mediated metabolic effects offer a durable, tolerable oral complement to incretin therapy, enabling sustained weight control across the lifetime of chronic disease.
Chronic oral PPARα axis
  • GLP-1 retention gap: only ~20% of patients remain on therapy after 2 years
  • Early drop-off: most patients discontinue within 3–6 months of starting
  • YPT adjunct positioning enables sustained weight control beyond the incretin window, with a durable oral add-on
Major commercial opportunity as a lifelong weight-control therapy positioned alongside incretin-based drugs.
Pipeline

A capital-efficient path to
candidate nomination.

A staged 18–30 month screening and preclinical workflow that moves from concept to validated lead candidate, with explicit, pre-defined go/no-go criteria at each milestone gate.

1
Library Design & CRO Synthesis
Rational design of BV-ester variants with AI/ML-guided prioritisation. CRO synthesis of initial 20–40 compound library.
Go criterion: ≥20 synthesizable BV-ester candidates with verified purity ≥95%.
4–6 mo
2
In Vitro Screening Campaign
Human serum esterase activity, membrane permeability assays (HepG2 and Caco-2), PPARα reporter, intracellular and extracellular BLVRA/BLVRB activity, bilirubin secretion activity.
Milestone 1
Go criterion: ≥3 compounds clearing permeability + esterase + PPARα activity thresholds.
3–6 mo
3
In Vivo Proof-of-Concept
Mouse APS model (MRL/lpr genetic model and aPL antibody induction).
Milestone 2
Go criterion: statistically significant disease-marker reduction vs. vehicle control in APS model.
6–12 mo
4
Non-GLP NHP PK/PD and Safety
Intra-animal dose escalation study to achieve target bilirubin range (50–100 μM) and assess safety before IIT or IND-enabling studies. IP filing covers composition of matter and method of use. Series A fundraise position.
Milestone 3
Go criterion: target plasma BR (50–100 µM) achieved with no dose-limiting toxicity in NHP.
1–6 mo
This seed round converts a compelling biological thesis into a de-risked drug program ready for Series A.
Competitive Landscape

Validated biology
despite limited direct competition.

The biology is increasingly validated, but the field remains open when it comes to building a chronic, oral therapy designed to safely recreate the protective bilirubin phenotype.

01 — Existing Approaches
Direct Bilirubin Therapeutics
External validation of the biology — but in a format that limits utility for chronic disease.
Bilix / BRIXELLE platform: PEGylated bilirubin, i.v., early clinical
Focused primarily on acute inflammatory indications
No approved or clinical-stage oral bilirubin-elevating therapy
02 — Unmet Need
Gap in the Field
The major unmet need remains a practical format for long-term use in chronic disease.
No approved or clinical-stage therapies designed to safely elevate bilirubin for chronic disease
i.v. and nanoparticle formats not suited for daily, long-duration administration
Oral prodrug chemistry not pursued by existing players
03 — Yellow Pigment
First-in-class oral approach
Pharmacologically recreating the Gilbert protective phenotype, designed for daily, chronic use.
Oral BV-ester prodrug platform with unique chemistry approach
Designed for chronic disease settings where duration and daily dosing matter
Human genetics-validated target with Gilbert syndrome as natural proof of concept
Existing field
Yellow Pigment
i.v. · acute · nanoparticle · early clinical
oral · chronic · prodrug · daily dosing
Strong external validation of the biology, with a clear gap around oral chronic-disease therapeutics.
Why Yellow Pigment

A platform built to convert protective biology
into category-defining medicines.

Yellow Pigment turns one of the strongest human protective phenotypes into a controlled, oral pharmacology platform, positioned to address some of medicine's largest unmet markets through three reinforcing pillars.

I
Human protective biology insight
A hypothesis grounded in one of the most replicated protective phenotypes in human genetics, already validated in millions of Gilbert carriers and not derived from cell lines or animal models alone.
Human genetics-validated target
Decades of consistent cohort evidence
Pleiotropic protection across disease areas
II
Controlled pharmacology through BV-ester prodrugs
A proprietary chemistry strategy that recreates the Gilbert protective window with controlled, oral, daily pharmacology, solving the delivery and formulation problem that has blocked prior bilirubin approaches.
BV-ester design library (40+ compounds)
Composition-of-matter IP opportunity
Oral, chronic, daily-dose format
III
Platform for major chronic-disease markets
A staged development engine that moves efficiently from screening cascade to validated candidate, with shared infrastructure unlocking commercial reach into multi-$10B+ metabolic, autoimmune, and inflammatory markets.
APS clinical entry → Metabolic / Obesity lead program
Cross-applicable tox and translational learnings
Capital-efficient path to Series A and partnership
Protective human biology · controlled oral pharmacology · multiple major chronic-disease markets — a platform positioned to define the bilirubin-elevation category.
Team & The Ask

Experienced founders raising seed capital
to reach a major inflection point.

Nikola Ivica
Nikola Ivica, PhD
Chief Scientific Officer
MIT PhD · Harvard BA. Deep expertise in heme metabolism, bilirubin biology, and therapeutic platform design. Scientific founder of the BV-ester hypothesis.
Ivan Posavec
Ivan Posavec
Chief Executive Officer
Harvard BA. Experienced CEO across multiple business domains and repeat biotech founder.
Luka Babić
Luka Babić
Chief Operating Officer
Harvard BA. Exited founder and operator focused on execution systems for complex ventures. Drives operational rigour across the platform build.
Advisors
Staša Stanković
Staša Stanković, PhD
OvartiX CEO, Cambridge PhD, AstraZeneca consultant, women's health scientist
Nenad Grmuša
Nenad Grmuša
DEM BioPharma CEO, former Takeda R&D strategy and external innovation leader
Seed Round
$1.5M
SAFE · 18-month runway
Synthesize and screen initial BV-ester library (40+ compounds)
Generate in vitro and in vivo proof-of-concept (APS + metabolic models)
Advance top candidates through early NHP tox work
Support IP filing for composition of matter and method of use
Goal: Nominate a Yellow Pigment development candidate and position the company for Series A financing or strategic partnering with a biopharmaceutical partner.
Key milestones funded
✓ Library design + CRO synthesis
✓ In vitro screening cascade
✓ In vivo efficacy (mouse APS + DIO)
✓ IP portfolio filing
→ Development candidate nomination