# Synthetic Cannabinoid Ajulemic Acid Shows Potent Antifibrotic Effects in Systemic Sclerosis Models

> **Author:** Benjamin Caplan, MD (ABFM Board Certified, MA Lic. #240562, NPI: 1962722637)
> **Publisher:** CED Clinic (https://cedclinic.com)
> **Canonical URL:** https://cedclinic.com/ajulemic-acid-antifibrotic-effects-systemic-sclerosis/
> **Published:** 2022-09-06T19:42:15-04:00 | **Last Modified / Clinically Audited:** 2026-09-28T11:16:27-04:00
> **Clinical Summary:** Discover how ajulemic acid antifibrotic effects target fibrogenesis in systemic sclerosis, offering new therapeutic potential without psychoactive effects.

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The therapeutic potential of cannabinoids such as THC is grossly limited by their psychoactive effects, leading to a growing interest in the development of synthetic analogs with similar benefits but without activity on the brain. One of such compounds is ajulemic acid (AjA), which can bind to both [cannabinoid receptors](https://cedclinic.com/citral-cannabinoid-receptor-2-activation-pain-relief/) and the peroxisome proliferator-activated receptor-γ (PPAR-γ) but can’t cross the [blood-brain barrier](https://cedclinic.com/thc-blood-brain-barrier-endocannabinoid-system-patience/) effectively to trigger psychoactive responses.

Recent evidence suggests a key role for [cannabinoid receptors](https://cedclinic.com/citral-cannabinoid-receptor-2-activation-pain-relief/) as well as PPAR-γ in fibrogenesis, which is the formation of fibrous tissue – a strong tissue consisting of twisted strands of collagens by cells known as fibroblasts. This process, when going unchecked, underlies diseases like systemic sclerosis, also known as scleroderma. More particularly, in systemic sclerosis, the uncontrolled fibrogenesis leads to chronic hardening and tightening of the skin and joint pain. For these reasons, scientists hypothesized that AjA could be a drug molecule targeting abnormal fibrogenesis in patients with scleroderma.

So far, several experiments have supported this hypothesis. First, AjA was found to strongly reduce collagen synthesis by scleroderma fibroblasts in skin cells from patients. This action was reversed completely in the presence of a PPAR-γ blocker, confirming that such reduction resulted from activation of PPAR-γ by AjA. Second, in murine models of scleroderma, when mice received AjA prior to induction of the disease process, abnormal thickening of the skin was significantly prevented. When mice received AjA 3 weeks into the disease, its progression was still moderately hindered.

If you or someone you know suffers from Scleroderma (or Crest Syndrome), and want to learn more about how cannabis may be helpful in providing relief, contact CED Clinic today at info@cedclinic.com. Dr. Caplan and his team would be happy to discuss treatment options.

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### Verification & Medical Governance

- **Lead Clinical Author:** Benjamin Caplan, MD
- **Credentials:** Board Certified in Family Medicine (ABFM), Former CMO Canna Care Docs (250,000+ patients supervised), Founder & CMO CED Clinic & CED Foundation, Author of *The Doctor-Approved Cannabis Handbook* (Penguin Random House).
- **Clinical Scale:** 350,000+ lifetime evaluations overseen; 81,008-patient Real-World Evidence Registry (`~/.ced_rwe_vault.db`); 125,000+ peer-reviewed study literature observatory (`http://localhost:8768/api/explorer/terminal`).
- **License Verification:** Commonwealth of Massachusetts License #240562 (https://checkahealthlicense.mass.gov/).
- **NPI Registry:** 1962722637 (https://npiregistry.cms.hhs.gov/provider-view/1962722637).
- **Ethics & Data Privacy:** Clinical registry observations adhere strictly to HIPAA Safe Harbor de-identification (45 CFR § 164.514(b)) and criteria for secondary research exemption under 45 CFR § 46.104(d)(4).
