According to the American Academy of Dermatology, 84.5 million Americans — one in four — are impacted by skin diseases. Skin diseases cost the US health care system $75 billion in medical, preventative, and prescription and non-prescription drug costs. Acne is the most common skin disease in the United States, affecting up to 50 million Americans annually.
Approximately 85 % of people between the ages of 12 and 24 experience at least minor acne. Over 25% of women and 12% of men in their 40s report having acne.
50% of women in their 20s,
33% of women in their 30s, and
25% of women in their 40s suffer from acne. Acne can affect more than your skin. Researchers have found in study after study that people with acne can also develop: depression, anxiety, low self-esteem, poor self-image, decreased quality of life, a feeling of being all alone. Although myriad acne treatments are available, current options may not be sufficient because of a lack of efficacy, limited tolerability, or burden of cost to patients. As patients become more concerned about the risks and side-effects of acne medications such as oral antibiotics and isotretinoin, other options are needed.
The paper "Innovation in acne treatment is long overdue but the treatment pipeline looks promising" was published in The Pharmaceutical Journal in 2017. At the start of this paper the author stated:
"There is no cure, and available treatments have significant drawbacks, yet there have been no novel products launched over the past 10 years — innovation is long overdue."
“For many years it’s been repurposing the same old stuff,” says Adam Friedman, a dermatologist at the George Washington University School of Medicine and Health Sciences, Washington. Unfortunately for millions acne sufferers this statement is still actual today, 7 years after this paper was published (look at current acne clinical trial landscape below).
CURRENT ACNE CLINICAL TRIAL LANDSCAPE
This is a snapshot of Phase I–IV clinical trials for primary investigational drugs with at least one industry sponsor in the acne space in
the curated Trialtrove database. There are equal proportions of clinical trials for acne across Phase I/II and Phase III/IV. Phase I/II and
Phase II/III trials are counted as Phase II and Phase III, respectively.
Forging a new standard in inflammatory dermatology.
Samdolite Pharmaceuticals is a science-driven dermatology company dedicated to redefining how inflammatory skin disease is treated. Built on deep mechanistic insight into innate immune activation, Samdolite is advancing a new generation of topical therapies designed to be potent without being punitive—effective without compromising skin health or systemic safety.
At the center of this vision is CromAzol™, Samdolite’s lead first-in-class topical anti-inflammatory therapy.
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On a mission to deliver power without punishment.
For decades, dermatology has relied on treatments that suppress, deplete, or overcorrect—often at the cost of tolerability or long-term safety. Samdolite was founded on a different belief: that precision modulation of inflammation, rather than blunt force suppression, is the key to durable skin health.
CromAzol™ is engineered to reversibly inhibit mast-cell– and neutrophil-driven inflammation upstream, addressing the biological drivers of acne, rosacea, and other inflammatory skin diseases—without systemic immune ablation or antibiotic dependence.
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Built for those who demand to understand.
Samdolite is designed for a new generation of dermatology stakeholders—clinicians, scientists, partners, and patients—who expect more than vague claims or recycled mechanisms.
These are individuals who ask:
• How does it work?
• What pathway is being targeted?
• Why should this be safer—and more effective—than what exists today?
CromAzol™ answers those questions through a mutual-prodrug architecture, quantifiable biological rationale, and a development strategy aligned with modern regulatory science.
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With therapies designed to deliver meaningful clinical impact.
CromAzol™ is not positioned as another incremental topical—it represents a platform approach to inflammatory dermatology. The same architecture supporting acne and rosacea is being extended to additional indications, including chronic urticaria, atopic dermatitis, and psoriasis.
Every Samdolite therapy is designed to:
• Address inflammation at its biological origin
• Be compatible with long-term use
• Integrate seamlessly into real-world dermatological care
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A name that reflects purpose.
CromAzol™ embodies Samdolite’s founding principles:
• Mechanism before marketing
• Efficacy rooted in biology
• Innovation guided by restraint, not excess
It reflects the belief that meaningful skin transformation begins with purposeful science, not overcorrection.
Rosacea is also our target.
Rosacea is a chronic inflammatory skin disease that affects 16 million Americans (The National Rosacea Society, http://www.rosacea.org/). Rosacea is a mast cell–derived disease. This statement is accepted by lead dermatologists.
Just read this article "Mast cells may play key role in rosacea pathogenesis"
“Once activated, the mast cells can promote the release of different mediators and have a considerable effect on the pathophysiology of diverse inflammatory diseases,” Dr. Wang et al.
“Mast cells appear to play an intricate role in the pathophysiology of rosacea and could serve as potential targets for future therapies, according to recent study findings.”
Read more information about rosacea and current and coming treatments for this disease in our APPROACH page.
New indication for SAMD-21 and SAMD-22
EGFR inhibitors are highly effective targeted therapies in several cancers, including colorectal, lung, pancreatic, and breast cancer, but dermatologic toxicity remains a major limitation. Papulopustular rash is the most common early skin adverse event, often emerging within the first 1–2 weeks of treatment and peaking around weeks 3–4. These eruptions can be severe enough to cause treatment interruption or discontinuation, even though they are often associated with better antitumor response.
Unlike acne vulgaris, these lesions are generally considered sterile inflammatory papules and pustules, typically without comedones. Pruritus can also be prominent, although incidence appears to vary considerably by drug.
Drug Variations: Itching occurs in approximately 18.2% to 54.9% of patients, with the lowest prevalence in those treated with cetuximab and the highest in those treated with panitumumab.
Breakdown by Specific EGFRi
Clinical data demonstrates a range of pruritus incidence based on the type of therapy used:
• Panitumumab: ~55%
• Gefitinib: ~18% to 20%
• Erlotinib: ~20% to 50%
• Cetuximab: ~18%
The current standard of care for rash treatment in patients undergoing EGFRi typically includes skin moisturizers, topical steroids, and antibiotics like minocycline or doxycycline that are administered prophylactically from the start of EGFRi therapy and are continued throughout the entire treatment period. If the rash continues to advance, oral steroids and/or antibiotics are administered. However, there are known systemic adverse events associated with these adjunctive therapies, and we believe that physicians and patients try to limit their use, particularly with oral antibiotics. Given the high incidence rate of rash that continues with these patients, as well as the concerns related to potential impacts of antibiotics on these therapies, we believe there is a clear unmet medical need for additional safe and effective adjunctive therapies for addressing papulopustular skin rash.
Current mechanistic hypothesis
From the literature, the currently emphasized mechanisms include:
• EGFR blockade in keratinocytes, with impairment of normal epidermal homeostasis
• induction of IL-36γ
• synergy with Cutibacterium acnes
• downstream activation of IL-8 and NF-κB
• resulting cutaneous neutrophilia
• impaired antimicrobial defense and increased susceptibility to S. aureus
This framework is very useful, but which role mast cells play in this process? May be they are acting even earlier in the inflammatory cascade, particularly in initiating or amplifying neutrophil recruitment.
Relevant therapeutic approaches already in development
Two examples are interesting:
• Hoth Therapeutics (HT-001)
A topical formulation of aprepitant, an NK-1 receptor antagonist. Mechanistically, this may reduce inflammation and itch by blocking the substance P / NK-1 pathway and thereby decreasing mast cell activation and degranulation.
• Azitra (ATR-04)
A live biotherapeutic approach using an engineered S. epidermidis strain selected for IL-36γ reduction and inhibition of S. aureus.
These programs suggest that the field is already moving toward more targeted approaches rather than relying only on oral antibiotics or general supportive care.
We have better solution for this problem
CromAzol, our topical mutual prodrug of cromoglicic acid and azelaic acid, and observed what appeared to be meaningful symptomatic improvement and local control of the rash. This mutual prodrug was designed for acne vulgaris and for rosacea. Azelaic acid function as anti-bacterial and anti-inflammatory compound. Cromoglicic acid inhibits mast cells and in addition cromoglycic acid (cromolyn sodium at pH 7-8) actively inhibits neutrophils. Research shows it suppresses neutrophils by:Inhibiting chemotaxis: it reduces the movement and migration of neutrophils toward inflammatory sites. It also prevents neutrophil activation and degranulation, which limits the release of tissue-damaging enzymes. Regulating Calcium: It lowers intracellular free calcium levels, a key step in activating neutrophils. In addition to its classic role as a mast cell stabilizer, cromoglycate acts directly on neutrophils to produce a broader anti-inflammatory effect.
Well, what if cancer patients have experience significant pruritus with either panitumumab or cetuximab?
CromCetol (SAMD-22) might be the more appropriate candidate for these patients. We designed more specifically for itch-dominant inflammatory skin conditions (chronic urticaria, prurigo nodularis). CromCetol that contains cromoglicic acid and cetirizine (Zyrtec) in form of prodrugs linked via ester bonds. All polar groups are blocked by ethyl esters. After esterase hydrolysis in viable layers of skin this mutual prodrug will release cetirizine (Zirtec) and alleviate itching/pruritus symptoms.
