AC-11 is an aqueous extract of the botanical, Uncaria 
tomentosa, which has a variety of effects that enhance 
DNA repair and down regulate inflammation. AC-11 is 
essentially free of oxindole alkaloids (< 0.05%, w/w) but 
contains more than 8% Carboxy Alkyl Esters (CAEs) as 
their active ingredients. Three groups of 10 outbred SK-1 
hairless or SK-II hairless strains of mice each were treated 
with AC-11 at 0.5%, 1.5%, and 3.0% in a non-irritating, 
dye-free, perfume-free, and fragrance-free vanishing cream 
vehicle. Ten mice used vehicle only and 10 were untreated. 
Each concentration of AC-11 and was applied daily to the 
backs of the mice prior to exposure to a 1,600-watt solar 
simulator used in this work (Solar Light Co. Philadelphia, 
PA) emitting (mainly Ultraviolet A (UVA) and B (UVB) 
radiation) duration of the experimental period with UVB 
wavelengths was filtered out with a 1.0 cm Schott WG 345 
filter. AC-11 with peak absorption at 200nm does act as a 
sun block. We tested for and focused on clinical 
appearance of mice and histological appearance of tumors 
in mice rather than metrics of radiation generated 
inflammation. Tumor progression scores were assigned as 
follows: 4+ = extensive tumor development; 3+ = early 
malignancies (raised palpable plaques) (early squamous  cell cancers) 2+ = firm scaling, palpable keratosis (actinic 
keratoses); 1+ = light scaling with erythema. Following a 
total cumulative dose of 738 J/cm2, 85.7% all of the 
irradiated control animals, which did not receive AC–11 
had precancerous actinic keratosis (AK)-type lesions (2+) 
(64.3% versus 42.9%) or early squamous cell carcinoma 
(SCC) (3+) (21.4% vs. 4.8%), in comparison with 47.7 % 
of AC-11-treated animals. There were no significant 
differences between the AC–11 groups. Three months 
after cessation of exposure to UVA radiation, the lesions 
in all but three of the 14 animals which were treated with 
AC-11 that were still evaluable irradiated with UVA 
radiation progressed to papillomas and frank squamous 
cell carcinomas (+4 responses). AC-11 retarded, but did 
not stop, carcinogenesis progression. It is possible that if 
AC-11 was continuously applied tumors would not have 
in mice treated with AC-11 for a limited period. While we 
do not know how AC-11 exerts its DNA repair and anti
inflammatory effects, AC-11 is therapeutic for the 
treatment at the time of development of actinic keratoses 
and squamous cell carcinomas in mice and by extension 
humans. Without the constant presence of AC-11 these 
protective effects do not occur.