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Clinical-stage · IBD

Redefining the treatment of inflammatory diseases

cAMPfield is a clinical-stage biopharmaceutical company focused on developing well-tolerated and highly effective oral medicines, founded and led by industry veterans with success developing therapies for immune-mediated inflammatory diseases, including inflammatory bowel disease (IBD).

Prifemilast is an investigational, potentially best-in-class, once-daily oral PDE4B-selective inhibitor designed to set a new standard of care for IBD. Prifemilast has been well-tolerated in more than 700 clinical trial participants to date and has demonstrated robust efficacy in a Phase 3 trial for plaque psoriasis. Many clinicians and patients prefer the convenience and familiarity of oral therapies, but currently approved oral treatments for IBD are limited by poor tolerability, safety concerns, or modest efficacy. Prifemilast offers the potential to combine the convenience of an oral therapy with the safety and efficacy that patients deserve. 

About us

The architects of today's standard of care

Founders

Executives who played key roles in the development or commercialization of Entyvio®, Humira®, Otezla® and Zeposia®

Mark Stenhouse, Chair, Board of Directors, cAMPfield Therapeutics

Mark Stenhouse

Chair, Board of Directors
Board Member — Phathom Pharmaceuticals
Prior experience
  • COO — Prometheus Biosciences (acquired by Merck for $11B)
  • VP US Immunology — AbbVie / Abbott
  • Led US sales and marketing for Humira®
Asit Parikh, MD PhD, Independent Board Member, cAMPfield Therapeutics

Asit Parikh, MD, PhD

Independent Board Member
CEO — MOMA Therapeutics
Board Member — Phathom Pharmaceuticals
Prior experience
  • SVP and Head of GI — Takeda
  • Led development of Entyvio® for IBD
  • Staff Gastroenterologist — Newton-Wellesley Hospital
LinkedIn
Keith Usiskin, MD, Interim Chief Medical Officer, cAMPfield Therapeutics

Keith Usiskin, MD

Interim Chief Medical Officer
Prior experience
  • VP, Head of GI — BMS / Celgene, Sanofi
  • Senior Director, Clinical Lead — Janssen
  • Led development of Otezla® and Zeposia® for IBD
LinkedIn

Mountainfield Venture Partners

Founder

A biopharma company creation firm building transformative companies around in-licensed drug candidates, world-class leadership teams, and syndicated capital raises from top-tier life science institutional investors.

Visit mountainfieldvp.com →

All third-party product names, company names, and logos are trademarks™ or registered® trademarks of their respective holders. Use of them does not imply any affiliation with or endorsement by them.

Leadership team

Significant experience successfully executing global clinical development programs

Bill Gerhart, MBA, Chief Executive Officer, cAMPfield Therapeutics

Bill Gerhart, MBA

Chief Executive Officer
Senior Advisor — Mountainfield Venture Partners
Board Member — Pulmovant
Prior experience
  • CEO — Kinevant, Respivant, Patara, Elevation, and Mpex Pharma
LinkedIn
David Socks, MBA, Chief Operating Officer and Co-founder, cAMPfield Therapeutics

David Socks, MBA

Chief Operating Officer, Co-founder
Managing Partner — Mountainfield Venture Partners
Prior experience
  • Venture Partner — Frazier Life Sciences
  • Co-founder of >15 biopharma companies, including 6 IPOs
  • 4-time CEO, including Phathom Pharmaceuticals
LinkedIn
Patricia Turney, MBA, Chief Technical Officer, cAMPfield Therapeutics

Patricia Turney, MBA

Chief Technical Officer
Prior experience
  • CTO — Acelyrin
  • SVP, Operations — Arcutis Biotherapeutics
  • VP, External Supply — Amgen
LinkedIn
John Kempen, MS, SVP, Clinical Development Operations, cAMPfield Therapeutics

John Kempen, MS

SVP, Clinical Development Operations
Prior experience
  • SVP, Head of Global Clinical Operations — Gossamer Bio
  • Director, Clinical Operations — Receptos / Celgene and Ardea Biosciences / AstraZeneca
  • Clinical Operations — Allergan, PPD, ICON
LinkedIn
Rita Shah, PharmD, VP, Regulatory Affairs, cAMPfield Therapeutics

Rita Shah, PharmD

VP, Regulatory Affairs
Prior experience
  • Sr. Director, Global Regulatory Strategy — Vertex Pharmaceuticals
  • VP, Global Regulatory Affairs — MBX Biosciences
  • Regulatory Affairs — AstraZeneca, Johnson & Johnson
LinkedIn
Christian Fougner, MD PhD, VP, Program Leader and Co-founder, cAMPfield Therapeutics

Christian Fougner, MD, PhD

VP, Program Leader, Co-founder
Prior experience
  • VP — Mountainfield Venture Partners
  • Management Consultant — McKinsey & Company
LinkedIn
Rayne Rodgers, MPH, Executive Director and Chief of Staff, cAMPfield Therapeutics

Rayne Rodgers, MPH

Executive Director, Chief of Staff
Prior experience
  • Head of Patient Advocacy / Recruitment — Roivant, Kinevant, and miRagen Therapeutics
  • VP — Muscular Dystrophy Association
  • Program Manager — Takeda
LinkedIn

Board of directors

Mark Stenhouse · ChaircAMPfield
Bill Gerhart, MBAcAMPfield
Aditya Kohli, PhDFrazier Life Sciences
Nanna Lüneborg, PhD, MBAForbion
Rebecca LuseDeep Track Capital
Asit Parikh, MD, PhDIndependent
David Socks, MBAcAMPfield / Mountainfield
Backed by
Mountainfield Venture Partners Frazier Life Sciences Deep Track Capital Forbion Abingworth
Venrock Longitude Capital Novo Holdings RA Capital
Our science

Validated mechanism + validated drug

Mechanism of Action

PDE4 inhibition in inflammatory bowel disease

cAMPfield is advancing prifemilast, a selective, once-daily oral inhibitor of phosphodiesterase 4B (PDE4B) for the treatment of IBD. PDE4 inhibition is a clinically validated mechanism in ulcerative colitis, and prifemilast has demonstrated best-in-class potential across more than 700 participants treated in clinical trials.

PDE4B inhibition mechanism of action in inflammatory bowel disease — adapted with permission from Silvio Danese. In IBD, low cAMP and active PDE4 drive immune infiltrate, pro-inflammatory cytokines, leukocyte recruitment, neutrophil chemotaxis and epithelial barrier disruption. PDE4B inhibition raises cAMP via PKA-CREB / Epac-Rap1, increasing anti-inflammatory cytokines, reducing leukocyte trafficking and neutrophil recruitment, and preserving epithelial barrier integrity — restoring mucosal homeostasis.
Adapted with permission from Silvio Danese.

Three lines of evidence that PDE4 inhibition works in IBD

01 · Mechanism
Inhibiting PDE4 helps restore balance to an overactive immune system by reducing multiple inflammatory signals that are known to drive IBD

Cyclic adenosine monophosphate (cAMP) is a key regulator of immune cell function and helps control inflammatory responses. PDE4 enzymes break down cAMP, reducing its anti-inflammatory effects. PDE4B, a PDE4 isoform predominantly expressed in immune cells, plays an important role in regulating inflammatory signaling. Therefore, selectively inhibiting PDE4B promotes cAMP signaling and helps reduce inflammation.1

Inhibiting PDE4B in IBD leads to an increase of intracellular cAMP, which in turn leads to:

  • Reduced production of pro-inflammatory cytokines (e.g., TNFα, IL-23)
  • Increased production of anti-inflammatory cytokines (e.g., IL-10)
  • Limited recruitment of immune cells to inflamed gut tissue and epithelial barrier improvement
  • Suppression of pro-fibrotic pathways
TNF ↓ IL-23 ↓ IL-10 ↑ Mucosal lymphocytes ↓
02 · Human genetics
Supported by human genetic evidence

When humans carry genetic variants that alter the same molecular pathway targeted by a drug, they represent a “natural experiment” that can provide valuable insight into the therapeutic and safety effects of modulating that pathway. In 2017, a genetic analysis of more than 35,000 individuals found that loss-of-function variants in the ADCY7 gene were associated with approximately a two-fold increased risk of ulcerative colitis.2

ADCY7 encodes an enzyme that generates intracellular cAMP, a key signaling molecule that helps regulate immune responses. PDE4 inhibition similarly increases cAMP levels, but by preventing its breakdown. Taken together, these findings suggest that reduced cAMP signaling increases susceptibility to ulcerative colitis, while enhancing cAMP signaling through PDE4 inhibition has the opposite effect and helps protect against the inflammatory processes that drive disease.

03 · Clinical trials
Validated in clinical trials

PDE4 inhibitors have been safe and efficacious in numerous clinical trials, leading to regulatory approvals in multiple immune-mediated inflammatory diseases, including plaque psoriasis, psoriatic arthritis, Behçet's disease, chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, and progressive pulmonary fibrosis.

Across multiple Phase 2 clinical trials, PDE4 inhibitors have also demonstrated the significant potential to effectively treat ulcerative colitis3-6; however, none have yet been advanced to Phase 3 trials or approval.

Citations
  1. Fanizzi F, Danese S. Article in press. 2026.
  2. Luo Y, et al. Nat Genet. 2017;49(2):186-192.
  3. Schreiber S, et al. Gastroenterology. 2007;132(1):76-86.
  4. Danese S, et al. Clin Gastroenterol Hepatol. 2020;18(11):2526-2534.e9.
  5. Jones C, et al. Presented at: UEGW. 2025 October 4.
  6. Peyrin-Biroulet L, et al. Presented at: DDW. 2026 May 5.
Prifemilast

A once-daily oral drug, selective for PDE4B, with more than 700 participants exposed

Prifemilast is a once-daily, oral PDE4B-selective inhibitor. Prifemilast has an extensive development history, including a completed Phase 3 trial in plaque psoriasis, supporting its potential to become a best-in-class oral therapy for IBD.

Overcoming the limitations of previous PDE4 inhibitors

While PDE4 inhibitors have been demonstrated effective for treating multiple diseases, their use has historically been limited by undesirable side effects. The side effects associated with previous PDE4 inhibitors are caused by1-4:

  • Inhibiting the PDE4D isoform as well as PDE4B
  • Penetration into the central nervous system
  • Extremely tight binding affinity and rapid absorption, causing an undesirably rapid increase of intracellular cAMP

Prifemilast more selectively inhibits the PDE4B subtype versus PDE4D. This selectivity is important because PDE4B is highly expressed in inflammatory immune cells and plays a central role in regulating the production of pro-inflammatory cytokines, whereas inhibition of other PDE4 subtypes, particularly PDE4D, has been associated with unwanted adverse effects.

In animal models, prifemilast has shown limited penetration into the brain. Additionally, prifemilast exhibits prolonged absorption, resulting in a slower rise in cAMP levels following dosing. Collectively, the enhanced selectivity, limited central nervous system penetration, and controlled absorption profile engineered into prifemilast are designed to improve tolerability relative to earlier PDE4 inhibitors. This may enable dosing that achieves optimal efficacy without the dose-limiting adverse events historically associated with the class.5

Best-in-class results in clinical trials

Prifemilast has an extensive development history, with more than 700 clinical trial participants exposed to date, including more than 250 participants with 52 weeks of exposure. Prifemilast was studied in a Phase 3 trial in plaque psoriasis, an immune-mediated inflammatory disease that shares overlapping pathobiology with IBD, including the IL-23/Th17 axis. The trial results demonstrate greater placebo-adjusted efficacy than has been reported to date for other PDE4 inhibitors. Prifemilast also demonstrated a compelling tolerability profile, with treatment discontinuation rates lower than those observed with placebo. Together, these findings provide clinical evidence that potent modulation of the PDE4/cAMP pathway can translate into meaningful therapeutic benefit in human inflammatory disease, supporting the potential for prifemilast to deliver differentiated efficacy in patients with IBD.5

700+ PARTICIPANTS EXPOSED 250+ PARTICIPANTS EXPOSED FOR >52 WEEKS PHASE 3 · PSORIASIS
Citations
  1. Fanizzi F, Danese S. Article in press. 2026.
  2. Spina D. British Journal of Pharmacology. 2008;155(3):308-315.
  3. Schafer PH, et al. Cellular Signalling. 2014;26(9):2016-2029.
  4. Peng T, et al. J Med Chem. 2020;63(19):10594-10617.
  5. Data on file (Newsoara); To-be-published.

Substantial human clinical experience has already been generated with prifemilast, supporting its potential to become a best-in-class PDE4 inhibitor for IBD.

Pipeline

Anchored by prifemilast

Our pipeline is anchored by prifemilast (HY1999/HPP737), a once-daily oral PDE4B-selective inhibitor for which we are initiating a global Phase 2b study in moderate-to-severe ulcerative colitis and a global Phase 2 study in moderate-to-severe Crohn's disease. Prifemilast is also being developed in plaque psoriasis in Greater China by cAMPfield's partner, Newsoara Biopharma Co., Ltd. (Newsoara).

Prifemilast
once-daily oral
PDE4B-selective
inhibitor
Indication
Preclinical
Phase 1
Phase 2
Phase 3
Filing
Ulcerative colitis
Global
Phase 2b · initiating
Crohn's disease
Global
Phase 2 · initiating
Plaque psoriasis
Newsoara · Greater China
Phase 3 · completed
News

Latest from cAMPfield

Company news, financing milestones, and clinical program updates. Visit the full newsroom →

June 18, 2026 · Launch

cAMPfield Launches With $180 Million Series A to Advance Prifemilast, a Potential Best-in-Class Oral Therapy for IBD

cAMPfield Therapeutics launched with a $180 million Series A financing to advance prifemilast, a once-daily oral PDE4 inhibitor in-licensed from Newsoara Biopharma, into global Phase 2 trials in moderate-to-severe ulcerative colitis and Crohn's disease. The financing was led by Frazier Life Sciences.

Read the launch announcement →
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