This clinical trial aims to investigate the efficacy of Calcipotriol ointment combined with 5-FU cream in Organ Transplant Recipients (OTRs) to determine if it can stimulate the immune cells against actinic keratoses precancerous skin lesions after transplantation and prevent cutaneous squamous cell carcinoma (SCC) in long-term.

Start Date01 Jan 2026

Sponsor / Collaborator

The General Hospital Corp.

[+1]

NCT04329221

/ WithdrawnPhase 2IIT

Calcipotriol Plus 5-Flourouracil Immunotherapy Before Transplantation for Skin Cancer Prevention in Organ Transplant Recipients

This clinical trial aims to investigate the efficacy of Calcipotriol ointment combined with 5-fluorouracil cream as an immunotherapy for actinic keratosis in Organ Transplant Recipients (OTRs) before transplantation and determine whether it can prevent cutaneous squamous cell carcinoma (SCC) in OTRs post-transplant.

Start Date01 Jan 2026

Sponsor / Collaborator

The General Hospital Corp.

[+1]

NCT06851507

/ RecruitingPhase 3

A Pilot Clinical Trial Comparing Topical Fluorouracil to Fluorouracil Plus Calcipotriene Field Treatments in Patients With Multiple Actinic Keratoses

The goal of this clinical research study is to compare the effects of topical fluorouracil alone to topical fluorouracil plus topical calcipotriene in patients with multiple actinic keratoses. "Topical" means the medication is applied directly to the skin.

Start Date06 Oct 2025

Sponsor / Collaborator-

100 Clinical Results associated with Calcipotriene

100 Translational Medicine associated with Calcipotriene

100 Patents (Medical) associated with Calcipotriene

1,869

Literatures (Medical) associated with Calcipotriene

01 Oct 2025·INTERNATIONAL IMMUNOPHARMACOLOGY

Myricetin alleviates DNCB-induced atopic dermatitis by modulating macrophage M1/M2 polarization

Article

Author: Xu, ZhiChang ; Zhang, XinJia ; Zhang, Yi ; Ma, RuiJu ; Li, Jing ; Wang, RuiRui ; Li, ChuYao ; Zhang, LiJuan ; Liu, YanJiao

BACKGROUND:

Atopic dermatitis (AD), a chronic and relapsing inflammatory skin disease, is characterized by recurrent eczema, itch, and pain. Conventional treatments, such as topical corticosteroids, are associated with various adverse effects. Previous studies have shown that Myricetin (Myr) effectively treats AD and inflammation induced by DNFB and MC903. However, the mechanism of Myricetin remains poorly understood. This study aims to investigate the therapeutic effects of Myricetin on DNCB-induced AD and to elucidate the underlying mechanisms.

METHODS:

An AD model was established with DNCB to evaluate the effectiveness of Myricetin by daily intraperitoneal injection at dosages of 2, 4, and 6 mg/kg. The Enzyme-linked immunosorbent assay (ELISA) was used for measuring levels of inflammatory cytokines/chemokines in ear tissues, Masson's staining was used to assess collagen loss, Immunofluorescence was used to identify macrophage infiltration in skin tissue, and Western blot was employed to detect the expression of proteins associated with M1 and M2 macrophage polarization. To investigate the underlying mechanism in vitro, RAW264.7 cells were employed for macrophage polarization analysis. M1 macrophages phenotype was induced with LPS + IFN-γ, whereas M2 macrophages phenotype was induced by IL-4. The Griess assay method was used to detect the content of NO, and the Enzyme-linked immunosorbent assay (ELISA) was used for measuring levels of IL-6, TNF-α, IL-1β, and IL-10 in M1 macrophage culture medium. Western blot was employed to detect the proteins expression of JAK1, JAK2, STAT1, IκB-α, P65, and iNOS in M1 macrophages. In M2 macrophages, Western blot was employed to detect the proteins expression of JAK1, JAK2, STAT1, STAT6, and Arg-1.

RESULTS:

Myricetin ameliorated skin lesions of DNCB-induced AD mice by reduced levels of pro-inflammatory chemokines/cytokines (IL-18, CXCL-9, CXCL-10), attenuated collagen loss in ear lesions, increased levels of the anti-inflammatory factors TGF-β1 and IL-10, increased the number of F4/80/CD206 positive cells and decreased the infiltration of F4/80/CD86 positive cells, suppressed iNOS protein expression and reduced the phosphorylation of STAT1, IκB-α, and P65, while enhancing Arg-1 expression and STAT6 phosphorylation. In vitro studies have demonstrated that Myricetin effectively suppressed the content of inflammatory factors such as IL-6, TNF-α, NO, and IL-1β, while elevating IL-10 concentration, reduced the proteins expression of p-JAK1, p-STAT1 (Tyr701), p-IκB-α, p-P65, and iNOS, in M1 macrophages. In M2 macrophages, Myricetin increased the expression of Arg-1 and phosphorylation of STAT6 protein expression, lowered the expression of phosphorylation of JAK1 protein expression.

CONCLUSIONS:

Our findings demonstrate that Myricetin significantly ameliorates skin lesions of DNCB-induced AD mice and reduces inflammatory factor levels by inhibiting the STAT1 and NF-κB signaling pathways to prevent M1 macrophage polarization, while activating the STAT6 signaling pathway to promote M2 macrophage polarization.

01 Sep 2025·ACTA HISTOCHEMICA

Calcipotriol inhibits the proliferation of psoriasis HaCaT cells by activating the ferroptosis pathway

Article

Author: Wu, Jiansong ; Yang, Lei ; Li, Chengxin ; Zhang, Jigang ; Wang, Lei ; Zhang, Yue ; Zhou, Li ; Liu, Shan

Calcipotriol is a well-established treatment for psoriasis and other dermatological conditions. This study aimed to investigate whether calcipotriol exerts its therapeutic effects through ferroptosis and to elucidate its underlying molecular mechanisms using bioinformatics and cellular experiments. Differentially expressed genes (DEGs) and their functional enrichment were analyzed in psoriatic skin lesions using bioinformatics. A lipopolysaccharide (LPS)-induced HaCaT cell model was established to simulate psoriatic inflammation. The effects of calcipotriol at various concentrations and time points on HaCaT cell proliferation, apoptosis, and expression of key markers were assessed. Additionally, ferrostatin-1 (a ferroptosis inhibitor) and RSL3 (a ferroptosis inducer) were used to evaluate ferroptosis-related changes, including cell proliferation, apoptosis, reactive oxygen species (ROS) levels, glutathione (GSH) content (via ELISA), and protein expression of GPX4 and Ki-67 (via Western blot). Bioinformatics analysis revealed significant differential expression of ferroptosis-related genes, such as GPX4 and SLC7A11, in psoriatic lesions. Calcipotriol treatment inhibited HaCaT cell proliferation in a dose- and time-dependent manner, elevated ROS levels, and reduced GSH, GPX4, and Ki-67 expression. These effects were reversed by ferrostatin-1, which restored antioxidant defenses and cell viability. Conversely, RSL3 increased ROS levels and partially negated the protective effects of ferrostatin-1. These findings suggest that calcipotriol regulates ferroptosis-related gene expression and inhibits keratinocyte proliferation through induction of oxidative stress and ferroptosis, offering new insights into its mechanism of action in psoriasis treatment.

01 Sep 2025·MOLECULAR AND CELLULAR BIOCHEMISTRY

The alleviating effect of Bai-Ju essence on atopic dermatitis through anti-inflammatory and skin barrier repair mechanisms

Article

Author: Chen, Ya ; Chen, Zhongjian ; Zhai, Chuntao ; Wu, Junchao ; Zhu, Quangang ; Zhu, Congcong ; Pan, Huijun ; Ma, Tianyou ; Tai, Zongguang

Bai-Ju essence (BJE) is a bioactive formulation composed of medicinal plant extracts, utilized in skincare products for its therapeutic potential. Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by epidermal barrier dysfunction and immune dysregulation. This study aimed to evaluate BJE anti-inflammatory and skin-protective effects, and its potential mechanisms in treating AD. The ability of BJE to restore the epidermal barrier was assessed in HaCaT cells. In LPS-induced RAW264.7 cells, the anti-inflammatory potential of BJE was evaluated by measuring NO, IL-6, PGE2, and TNF-α. Western blot analysis was used to assess the regulation of the MAPK pathway. An in vivo AD-like mouse model was established using MC903, and measurements of body weight, ear thickness, and AD symptoms were recorded. Histological analysis quantified mast cell infiltration, while western blot determined FLG, LOR, and ELOVL6 expression. ELISA was used to measure TNF-α, IgE, IL-4, and IL-13 levels. Flow cytometry assessed the effect of BJE on Th cell phenotypes. BJE significantly enhanced skin barrier protein expression (CERS2, LOR, HAS-1, HAS-2, FLG) in HaCaT cells. It significantly reduced the levels of NO, IL-6, PGE2, and TNF-α in LPS-treated RAW264.7, demonstrating its anti-inflammatory potential. Mechanistically, BJE inhibited MAPK activation. BJE decreased ear thickness, improved skin lesions, and relieved AD symptoms in AD-like mice. In addition, BJE effectively suppressed mast cell infiltration and hyperkeratosis. BJE also decreased levels of TNF-α, IgE, IL-4, and IL-13 while increasing LOR, ELOVL6, and FLG expressions. Furthermore, BJE modulated Th1, Th2, and Th17 cell proportions. BJE promoted epidermal barrier repair in HaCaT, suppressed the LPS-induced inflammation in RAW264.7, enhanced the skin barrier integrity in AD-like mice, and exhibited immunomodulatory effects by restoring Th cell balance. These findings highlighted the therapeutic potential of BJE in AD through its dual action of anti-inflammation and skin barrier restoration.

News (Medical) associated with Calcipotriene

07 Nov 2025

·www.prnewswire.com

ACAAI 2025 | CS2015 (OX40L/TSLP Bispecific Antibody) Makes International Debut

SUZHOU, China, Nov. 6, 2025 /PRNewswire/ -- CStone Pharmaceuticals ("CStone," HKEX: 2616), an innovation-driven biopharmaceutical company focused on the research and development of therapies for oncology, autoimmune/inflammation, and other key disease areas, today announced that the Company will present one of its autoimmune and inflammation pipeline assets, CS2015 (OX40L/TSLP bispecific antibody), in the format of an ePoster plus an on-site oral presentation at the 2025 Annual Scientific Meeting of the American College of Allergy, Asthma & Immunology (ACAAI). ACAAI is one of the most influential academic conferences in the fields of allergies, asthma, and immunology, attracting experts and scholars around the world to discuss the latest scientific advancements. This marks the first presentation of CS2015 at an international academic conference. The full content of the abstract and eposter is now officially available on the ACAAI website. Key highlights of the presentation: CS2015 features an asymmetric molecular design that simultaneously targets OX40L and TSLP, two clinically validated critical regulators of type 2 inflammation. The molecule incorporates an engineered Fc region with reduced binding affinity for FcγR, which extends its in vivo half-life and optimizes its pharmacokinetic (PK) profile to support long-term dosing intervals. CS2015 also exhibits excellent molecular stability, facilitating the development of high-concentration subcutaneous formulations. Its strong developability profile further supports high-yield and scalable manufacturing. 1. Dual Blockade: CS2015 lead molecule demonstrated potent inhibition of OX40L/OX40 and TSLP/TSLPR downstream signaling: CS2015 potently interrupted the engagement of hOX40L on hOX40 reporter cells and hTSLP on hTSLPR/IL-7Rα reporter cells, respectively; The blocking activities of CS2015 were comparable to those of benchmark (parental) antibodies, with single or sub nanomolar IC50s. 2. Robust Inhibition of Inflammatory Responses: CS2015 lead molecule inhibited the release of inflammatory cytokines from primary CD4+ T cells stimulated by TSLP/OX40L and suppressed TSLP-induced release of TARC (CCL17) in human monocytes and peripheral blood mononuclear cells (PBMC). 3. Early Signs of Efficacy: CS2015 demonstrated potent disease control activities in Atopic Dermatitis (AD) model with OX40 and TSLP humanized mice. In MC903-induced AD models, CS2015 lead molecule: Rapidly reduced skin lesion severity including ear and epidermal thickening; Decreased immune cells, especially mast cells infiltration; Reduced itch events. 4. Durability Advantage: CS2015 demonstrated superb PK profiles in Non-Human Primate (NHP), supporting long-term dosing intervals: CS2015 lead molecule K19LS exhibited a mean half-life of 21 days (504.6 hours, Subcutaneous [SC]) and 25.7 days (617.6 hours, Intravenous [IV]); K19LS had a clearance rate of 2.4 (SC) and 2.7 (IV) ml/day/kg, and was well-absorbed, with outstanding bioavailability. 5. Outstanding drug-like properties: Beyond the data shown in the poster, CS2015 further demonstrated: Outstanding accelerated stability under high-temperature stress (40°C); Low viscosity (scored at only 3.7 for a 100 mg/ml solution), promising for subcutaneous injection at high-concentration; Potent efficacy in the intranasal OVA/TSLP-induced asthma model by decreasing the secretion of IL-4, CCL17, IgE, etc., and alleviating pulmonary pathological changes. CStone will further advance the development of CS2015 to treat Th2 cell-mediated inflammation diseases, including AD, asthma, hidradenitis suppurativa (HS), chronic obstructive pulmonary disease (COPD), Chronic Rhinosinusitis with Nasal Polyps (CRSwNP), etc. The presentation schedule is as follows: Title: CS2015 a TSLP/OX40L Bispecific Antibody as a Potential Novel Therapeutic Agent for Type 2 Inflammation Diseases Presentation Type: ePoster display & 15-min on-site oral presentation (ePoster ID: R377) Abstract ID: 8079 Date & Time: Friday, November 7, 3:05 PM ET Location: ePoster Area of the West Exhibit Hall, Monitor 22 *The abstract and ePoster have been officially available on ACAAI website: . About CStone CStone (HKEX: 2616), established in late 2015, is an innovation-driven biopharmaceutical company focused on the research and development of therapies for oncology, autoimmune/inflammation, and other key disease areas. Dedicated to addressing patients' unmet medical needs in China and globally, the Company has made significant strides since its inception. To date, the Company has successfully launched 4 innovative drugs and secured approvals for 16 new drug applications covering 9 indications. The company's pipeline is balanced by 16 promising candidates, featuring potentially first-in-class or best-in-class antibody-drug conjugates (ADCs), multispecific antibodies, immunotherapies and precision medicines. CStone also prides itself on a management team with comprehensive experiences and capabilities that span the entire drug development spectrum, from preclinical and translational research to clinical development, drug manufacturing, business development, and commercialization. For more information about CStone, please visit: . Forward-looking statements The forward-looking statements made in this article only relate to events or information as of the date when the statements are made in this article. Except as required by law, we undertake no obligation to update or publicly revise any forward-looking statements, whether as a result of new information, future events or otherwise, after the date on which the statements are made or to reflect the occurrence of unanticipated events. You should read this article completely and with the understanding that our actual future results or performance may be materially different from what we expect. All statements in this article are made on the date of publication of this article and may change due to future developments. Disclaimer: only for communication and scientific use by medical and health professionals, it is not intended for promotional purposes. SOURCE CStone Pharmaceuticals 21% more press release views with Request a Demo

AACRClinical Result

10 Jun 2025

·www.prnewswire.com

DeepCure Announces DC-15442 as Development Candidate, an Oral STAT6 Inhibitor with 100% in vivo inhibition of pSTAT6 and comparable efficacy to dupilumab across disease models

DC-15442 is a potent small molecule STAT6 inhibitor, which is not a degrader or prodrug, being advanced as a safe dupilumab-in-a-pill alternative for patients BOSTON, June 10, 2025 /PRNewswire/ -- DeepCure, an immunology therapeutics company leveraging artificial intelligence (AI) to rapidly advance novel small molecule drugs, today announced the nomination of DC-15442 as its second development candidate. DC-15442 is a potent, selective, oral STAT6 inhibitor designed to replicate the safety as well as the efficacy of dupilumab, without requiring regular subcutaneous injections. Dupilumab is FDA-approved for multiple indications driven by Type 2 inflammation, including atopic dermatitis, asthma, chronic obstructive pulmonary disease (COPD), chronic rhinosinusitis with nasal polyps, chronic spontaneous urticaria, eosinophilic esophagitis, and prurigo nodularis. DeepCure designed DC-15442 to meet the demand for an oral alternative that is not only equally effective as dupilumab, but also has excellent safety, given that many patients are children and reproductive-aged adults with chronic, non-life-threatening conditions. DC-15442 inhibits the same IL-4/IL-13 signaling pathway as dupilumab by blocking the interaction between unphosphorylated STAT6 (uSTAT6) and the IL-4Ra receptor, and by preventing nuclear translocation and dimerization of phosphorylated STAT6 (pSTAT6). Importantly, like dupilumab, DC-15442 does not degrade STAT6 proteins or impair uSTAT6 non-inflammatory functions. Therefore, DC-15442 does not have the on-target safety concerns of potential therapies based on STAT6 degradation. In preclinical evaluations, DC-15442 achieved nearly 100% inhibition of pSTAT6 in the acute ovalbumin (OVA) allergy models, which outperforms IL-4Ra antibodies and other STAT6 inhibitors. In direct comparisons using the MC903 atopic dermatitis model, DC-15442 matched dupilumab's effectiveness, significantly reducing serum IgE levels to those seen in healthy controls. Additionally, DC-15442 has a dramatic effect on lung function in asthma models, restoring lung function to almost the same levels as healthy controls, with an effect superior to a leading JAK inhibitor (upadacitinib) and dexamethasone. The development candidate also exhibits outstanding selectivity, showing no off-target activity across extensive screening panels - including 102 SH2 domain proteins, 468 kinases, and 78 assays targeting clinical adverse drug reaction-associated proteins. Preliminary in vivo safety assessments confirmed outstanding tolerability, with no observed adverse effects, underscoring its suitability for chronic use. In addition, DC-15442 is not a degrader, and therefore it does not have the potential toxicity concerns of PROTACs. "We are extremely pleased that, in addition to excellent efficacy, DC-15442 demonstrates a very clean safety profile," said Kfir Schreiber, CEO & Co-Founder, DeepCure. "Many of the patients who will consider an oral STAT6 inhibitor will need to have chronic treatment for non-life-threatening conditions, so safety is paramount. As a selective, oral inhibitor that replicates dupilumab's proven mechanism without the target and modality risks associated with protein degradation, DC-15442 may expand the treated population and transform patient quality of life." About DeepCure DeepCure was founded by researchers at MIT to accelerate breakthrough therapies using artificial intelligence (AI) and advanced physics simulations to innovate small molecule discovery. The company is based in Boston, MA, and its engineers, chemists, and biologists collaborate on hard problems to find solutions that will have an enormous impact on patient health. For more information, visit . Contact [email protected] SOURCE DeepCure WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

Drug ApprovalClinical Result

28 Mar 2025

·pmlive.com

LEO and Reig Jofre partner to improve access to psoriasis therapy in Europe

L-R: Ignasi Biosca, CEO of Reig Jofre, and Juan Fran Cuello de Oro, general manager of LEO Pharma Iberia LEO Pharma and Reig Jofre have entered into a partnership aimed at improving access to LEO’s psoriasis treatment in Europe. The commercial agreement will focus on strengthening the promotion of Enstilar, an aerosol spray foam containing the vitamin D analogue calcipotriol and betamethasone dipropionate, for mild-to-moderate psoriasis within the scope of primary care across Spain. Approximately 125 million people worldwide are affected by some form of psoriasis, a chronic inflammatory condition that typically affects the skin, nails and joints. Up to 90% of patients have plaque psoriasis, characterised by distinct round or oval plaques typically covered by silvery-white scales. LEO’s fixed-dose combination therapy is designed to improve anti-psoriatic response in patients and has been recognised by Farmaindustria, the national association of the pharmaceutical industry in Spain, as an “incremental innovation” due to its advanced foam-based formulation. The collaboration between LEO and Reig Jofre will help extend the treatment’s reach, improve patient access and enhance support for healthcare professionals. “This agreement marks a significant milestone in positioning Reig Jofre and LEO Pharma as key players in medical dermatology in Spain,” Reig Jofre outlined in a statement, adding that the partnership “ensures that healthcare professionals receive the support, proximity and information needed to provide the best possible care to their patients”. LEO has already entered into a number of partnerships this year. Last month, it announced a collaboration with non-profit organisation DEBRA Research aimed at accelerating the development of treatments for epidermolysis bullosa, a group of rare and painful inherited skin disorders that cause the skin to become very fragile and tear or blister very easily. Though financial details of the alliance were not disclosed, the partners said they are hoping to “enhance scouting capabilities and provide additional capacity to accelerate the development of life-changing therapies for epidermolysis bullosa”. The company also partnered with Gilead Sciences in January to advance its small molecule oral STAT6 programme for inflammatory diseases. The deal, worth $1.7bn, gave Gilead global rights to develop, manufacture and commercialise the oral STAT6 programme. Meanwhile, LEO will hold exclusive global rights to STAT6 topical formulations in dermatology, and will have the option to co-commercialise oral programmes for dermatology indications outside the US.

License out/in

100 Deals associated with Calcipotriene

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KEGG	Wiki	ATC	Drug Bank
D01125	Calcipotriene	D05AX02	DB02300

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Psoriasis	China	LEO Pharmaceutical Products OOO	07 Aug 2001
Psoriasis vulgaris	Japan	Leo Pharma, Inc.	18 Jan 2000
Plaque psoriasis	United States	LEO Pharma A/S	29 Dec 1993

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Psoriasis of scalp	Phase 3	Canada	Leo Pharma, Inc.	01 Nov 2004
Psoriasis of scalp	Phase 3	Denmark	Leo Pharma, Inc.	01 Nov 2004
Psoriasis of scalp	Phase 3	France	Leo Pharma, Inc.	01 Nov 2004
Psoriasis of scalp	Phase 3	Norway	Leo Pharma, Inc.	01 Nov 2004
Psoriasis of scalp	Phase 3	Portugal	Leo Pharma, Inc.	01 Nov 2004
Psoriasis of scalp	Phase 3	Spain	Leo Pharma, Inc.	01 Nov 2004
Psoriasis of scalp	Phase 3	Sweden	Leo Pharma, Inc.	01 Nov 2004
Psoriasis of scalp	Phase 3	United Kingdom	Leo Pharma, Inc.	01 Nov 2004
Arthritis, Psoriatic	Phase 2	France	Leo Pharma, Inc.	01 Apr 2015
Dermatitis, Atopic	Phase 2	Canada	Leo Pharma, Inc.	01 Oct 2006

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


EADV2022	Phase 3	Plaque psoriasis	-	Calcipotriene (CAL) and betamethasone dipropionate (BDP) cream	nfbzounfpp(lkxfdlfwef) = oxmkgqrqnt azqlqmwhcu (erllyvlzoy ) View more	-	07 Sep 2022
				Vehicle	nfbzounfpp(lkxfdlfwef) = xyuwwrhkuw azqlqmwhcu (erllyvlzoy ) View more
EADV2022	Phase 3	Psoriasis of scalp	-	CAL/BDP cream	lofesrbkhx(xgzcuutjvd) = clcluwwvfi bpbtdocjlu (jogwofrjxp ) View more	-	07 Sep 2022
				Vehicle cream	lofesrbkhx(xgzcuutjvd) = phvubhwocu bpbtdocjlu (jogwofrjxp ) View more
phase 3 (EADV2022)	Phase 3	Plaque psoriasis	796	Calcipotriene and betamethasone dipropionate cream	dmzbdlgrnu(drskaqetdy) = icacqywpxu nffqcawwal (wtvxushqss ) View more	Positive	07 Sep 2022
				Calcipotriene and betamethasone dipropionate gel	dmzbdlgrnu(drskaqetdy) = ocybbzwcbl nffqcawwal (wtvxushqss ) View more
Pubmed Manual	Not Applicable	Psoriasis vulgaris	166	Calcipotriene+LEO90100	peuvvlagjb(slochebtkk) = ruhysysnof djsugmolgv (narcwwckrc, 3.0) View more	Positive	18 Jul 2022
NCT00704262 (CTgov)	Phase 2	Psoriasis vulgaris	33	LEO 80190+Calcipotriol+hydrocortisone	cgxyhotkoa = crmpmizqzp cleihplggn (pdnmhirvnv, xpysvlplsf - jsklsaawgb) View more	-	20 Oct 2020
NCT01694433 (CTgov)	Phase 2/3	Acne Vulgaris	66	Calcipotriene (Calcipotriene Cream)	cnicmappdg(jxekwuqlep) = rmndeqzofn wikpesiakl (zwwlkwhyhu, rndygjztio - qlzlpeeoeg) View more	-	07 May 2019
				Placebo (Placebo)	cnicmappdg(jxekwuqlep) = npgjntdvtl wikpesiakl (zwwlkwhyhu, imkqhrotlf - ejpbeehjig) View more
NCT02411643 (CTgov)	Early Phase 1	Scleroderma, Localized	2	topical calcipotriene 0.005% ointment	unqzxmzyid(tbkeqpjrrg) = aoleuvwfzk phlbkursml (ptttjplchf, oiutpxzwvs - qevdqgonal) View more	-	13 Sep 2018
NCT00656019 (CTgov)	Phase 2	Breast Cancer	63	Vitamin D (Normal Vitamin D Levels)	nampwotrba = nrepxtxufi oxfbpilrrg (fodaxawcix, agasfdglwc - jlgzvnciph)	-	02 Dec 2017
				Vitamin D (Low-normal Vitamin D Levels)	nampwotrba = ixdeionrxh oxfbpilrrg (fodaxawcix, guwvnacgka - kkwmebwvqa)
NCT02132936 (PSO-ABLE, Pubmed \| Am J Clin Dermatol)	Phase 3	Psoriasis	504	Cal/BD foam	hzvedshboz(wnnhmekgnd) = wfjzaujtaq zbhyolfhbw (bcyngbiefn ) View more	-	01 Jun 2017
				Cal/BD gel	hzvedshboz(wnnhmekgnd) = jnwsbuaobb zbhyolfhbw (bcyngbiefn ) View more
NCT01745133 (CTgov)	Phase 4	Plaque psoriasis	63	vehicle foam	bfwexwfynp(gdixaffnpt) = auqxjwjwct vtippfgifp (lufplyyvgk, ryeimqzpid - kfegpwfncv) View more	-	17 Nov 2016

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